Learning Objectives: AH1 Cardiology Flashcards
(136 cards)
1
Q
Differential diagnosis for chest pain:
think: Cardiac, pulmonary, GI, vascular, mediastinal, MSK, MH other
A
2
Q
Loss of consciousness: Differential diagnosis? (list 8)
Think- due to true syncope- (impaired cerebral blood flow) Vs Loss of consciousness due to impaired cerebral perfusion!
A
3
Q
Differential for local edema, Generalised oedema?
List 4 for both
A
Generalized oedema ddx:
- increased hydrostatic pressure/fluid overload ■ HF, pregnancy, drugs (e.g. CCBs), iatrogenic (e.g. IV fluids)
- decreased oncotic pressure/hypoalbuminemia ■ liver cirrhosis, nephrotic syndrome, malnutrition
- increased interstitial oncotic pressure— myxedema
- increased capillary permeability ■ severe sepsis
- hormonal ■ hypothyroidism, exogenous steroids, pregnancy, estrogens
4
Q
Differential diagnosis for Palpitations? - think causes of sinus tachy, then pathological tachycardias,
Differential diagnosis for dyspnoea? (Excercise, CVS, resp, parenchymal lung disease, pulmonary vascular, neurovascular, anxiety, haem/metabolic
A
5
Q
ACS: ST elevation myocardial infarction:
How are the patients likely to present?
What should be done immediatley in pt with suspected ACS?
How do you make a clinical diagnosis of ACS? (e.g what bloods and ECG requirements)
What is the best management strategy for ACS if a patient is close to a teritary hospital?
What should all patients who survive and Acute MI
A
- ST-elevation myocardial infarction (STEMI) presents with central chest pain that is classically heavy in nature, like a sensation of pressure or squeezing. Examination is variable, and findings range from normal to a critically unwell patient in cardiogenic shock.
- Give a loading dose of aspirin as soon as possible to any patient with suspected acute coronary syndrome.
- Make a clinical diagnosis of STEMI and start immediate treatment when a patient presents with symptoms suggestive of myocardial ischaemia and has persistent ST-segment elevation in at least 2 anatomically contiguous ECG leads.
- A rise in cardiac-specific troponins confirms the diagnosis but do not wait for laboratory results before starting treatment.
- Immediate and prompt reperfusion can prevent or minimise myocardial damage and improve the chances of survival and recovery. Primary percutaneous coronary intervention (PCI) is the best management option for most patients, with fibrinolysis reserved for those without access to timely primary PCI.
- Survivors of acute MI should receive cardiac rehabilitation and be closely followed up to ensure adequate modification of risk factors and optimisation of (and adherence to) pharmacotherapy for secondary prevention, and to monitor for the development of post MI complications and/or residual angina symptoms
6
Q
What is the definition of ACS? (e.g what is the STEMI requirements)
A
- Acute myocardial infarction is myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand. In the case of ST-elevation myocardial infarction (STEMI) this is caused predominantly by complete atherothrombotic occlusion of a coronary artery.
- In the appropriate clinical context, a STEMI is diagnosed clinically when there is new (or increased) and persistent ST-segment elevation in at least two contiguous leads of ≥1 mm in all leads other than leads V2-V3 where the following cut-off points apply:
- ≥2.5 mm in men <40 years old
- ≥2 mm in men >40 years old
- ≥1.5 mm in women regardless of age
- 1 mm = 1 small square (at a standard ECG calibration of 10 mm/mV).
Contiguous ECG leads lie next to each other anatomically and indicate a specific myocardial territory
7
Q
What are the major risk factors for ACS?
A
8
Q
What is the Aetiology of MI?
What is the pathophysiology?
A
Aetiology
- MI is usually a consequence of coronary artery disease. Atherosclerosis with plaque fissuring or rupture and thrombus formation is the underlying aetiology for STEMI in most patients. A small proportion of patients present with STEMI caused by coronary spasm reducing myocardial perfusion, coronary embolism, or following chest trauma or spontaneous coronary or aortic dissection.
Pathophysiology
- Atherosclerotic plaques form gradually over years
- They begin with the accumulation of low-density lipoprotein cholesterol and saturated fat in the intima (the inner layer) of blood vessels.
- This is followed by the adhesion of macrophages to endothelium, then diapedesis and entry into the intima, where they accumulate lipids and become foam cells.
- Foam cells are a rich source of proinflammatory mediators.
- The lesion up to this point is referred to as a fatty streak, and may be reversible to a certain extent.
- Subsequent evolution involves migration of smooth muscle cells from the media, and their proliferation and deposition of extracellular matrix, including proteoglycans, interstitial collagen, and elastin fibres.
- Some of the smooth muscle cells in advanced plaques exhibit apoptosis.
- Plaques often develop areas of calcification as they evolve.
- The plaque initially evolves with the artery remodelling outwards, followed by encroachment on the arterial lumen. Eventually the stenosis can limit flow under conditions of increased demand, causing angina.
STEMI typically occurs after abrupt and catastrophic disruption of a cholesterol-laden plaque. This results in exposure of substances that promote platelet activation and aggregation, thrombin generation, and thrombus formation, causing interruption of blood flow. If the occlusion is severe and persistent, myocardial cell necrosis follows.
- On interruption of blood flow in the coronary artery, the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work.
- Early hyperkinesis of the non-infarcted zones occurs, probably as a result of acute compensatory mechanisms including increased sympathetic activity and Frank-Starling mechanism. As necrotic myocytes slip past each other, the infarction zone thins and elongates, especially in anterior infarction, leading to infarction expansion.
- If a sufficient quantity of myocardium undergoes ischaemic injury, left ventricular (LV) systolic function becomes depressed; cardiac output, stroke volume, blood pressure, and compliance are reduced; and end systolic volume increases.
- Clinical heart failure occurs if 25% of myocardium has abnormal contraction, and cardiogenic shock occurs on loss of >40% of LV myocardium.
- Decreased compliance and increased LV end diastolic pressure give rise to diastolic dysfunction.
9
Q
How are MIs Classified?
What is the “Fourth Universal Definition of myocardial infarction”? (acute MI Types 1,2,3) What implications do each of these classifications have on management (they are different..)
A
Acute coronary syndrome (ACS)
- Historically ACS has been divided into three clinical categories according to the presence or absence of ST-segment elevation on a presenting ECG and on elevations of cardiac troponin T or I.
- ST-elevation myocardial infarction (STEMI): ECG shows persistent ST-segment elevation in at least two anatomically contiguous leads.
- Non-STEMI (NSTEMI): ECG does not show ST-segment elevation, but cardiac biomarkers are elevated. The ECG may show ischaemic changes such as ST-segment depression, T-wave inversion, or biphasic T waves.
- Unstable angina pectoris: non-specific ischaemic ECG changes, but cardiac biomarkers are within the normal range.
10
Q
Case examples of ACS:
A
11
Q
Outline some key recommendations for Urgent assessment and diagnosis of STEMI:
A
12
Q
What is the classification of Cardiogenic shock?
A
13
Q
What are important differentials to consider with pt presenting with chest pain?
A
Always consider alternative diagnoses that might explain the presenting symptoms and/or ST elevation on ECG, including:
- Aortic dissection (ST elevation can be present on the ECG)
- Pulmonary embolism (ST elevation or ST depression can be present on the ECG)
- Pericarditis (ST elevation can be present on the ECG)
- Myocarditis (ST elevation can be present on the ECG)
- Pneumothorax
- Pneumonia
- Intracranial pathology (e.g., subarachnoid haemorrhage)
- Gastro-oesophageal reflux disease
- Oesophageal spasm
- Costochondritis
- Anxiety or panic.
14
Q
Outline ECG leads associated with each vessels:
Lateral circumflex-
Inferior RCA
Septal (LAD) -
Anterior (LAD)
Lateral circumflex or diagonal
A
15
Q
How can a previous”silent MI’ be diagnosed?
A
16
Q
Anterior STEMI ECG
-Example key fetaures?
A
17
Q
Aneterolateral STEMI example:
Key features?
A
18
Q
Inferoposterior STEMI
Key features ECG?
A
19
Q
What are key features on hx and examination for ACS?
A
20
Q
What are key investigations to undertake in patient with suspected ACS?
A
21
Q
DDx for ACS?
A
22
Q
Criteria for ACS - ST elevation ECG?
Criteria for acute, evlovling or recent MI?
Criteria for established MI?
A
23
Q
ACS Qld Health clinical pathway page 1:
A
24
Q
ACS Qld Health clinical pathway page: Day 1 Pathway (Acute STEMI/NSTEMI)
Investigations?
Medications?
Observations/Treatments? (how often and what and why)
Nutrition and mobility?
Education and discharge planning?
A
25
Qld Health treatment pathway unstable angina/Late presentation MI:
Investigations?
Medications and pain management?
Observations and treatments?
Nutrition/mobility?
Education/discharge planning?
26
Management pathway QLD health 24 hours post inital management: (inpatient guidelines)
Treatments?
Observations?
Education?
27
Thrombolysis pathway QLD health:
What are indications for thrombolysis?
What are absolute contraindications to thrombolysis?
What are relative contraindications to thrombolysis?
28
Outtline management for thrombolysis according to QLD health pathway:
- Observations/ e.g IV access x2
- Treatments (medications including thrombolytic agent)
- Ongoing management
29
Management principles for STEMI/PCI avaliable:
Medications/Supportive management and assessments?
30
What primary CVD prevention techniques should be implemented in all patients?
Secondary prevention?
31
Complications of ACS?
32
CHF:
What are non pharmaological Preventitive strategies for HF?
33
Prevention of heart failure- pharmological?
What agents are shown to have preventive benefits for HF?
34
What investigations are recommended for diagnosis of HF?
* 12 lead ECG - Assess cardiac rhythm, QRS duration, and presence of underlying ischaemia or LV hypertrophy
* CXR: recommended in new HF- to detect signs of pulmonary congestion and identify alternative cardiac or non cardiac for pts symptoms
* Plasma BNP or proBNP- recommended for diagnosis in pts with HF
* Transthroracic echocardiogram- to improve diagnostic accuracy and in new patients to assess cardiac structure and function- including the measurement of LV ejection fraction (to classify diagnosis- which will dictate management
* Coronary angiography or Cardiac magnectic resonance imaging (CMR) should be considered in patients with low to intermediate pretest probability of CAD, to distinguish ischaemic and non ischaemic causes of ventricular dysfunction
* Non invasive function testing- Stress echocardiography, single photon emission CT (SPECT) /PET
* CMR with LGE should be considered in patients with heart failure associated with increased LV wall thickness that remains unexplained following clinical evaluation, including a 12-lead ECG and echocardiogram to identify inflammatory and infiltrative cardiomyopathies
* Either PET or bone scintigraphy may be considered in patients with heart failure associated with increased LV wall thickness that remains unexplained following clinical evaluation, including a 12-lead ECG and echocardiogram to identify infiltrative cardiomyopathies.
* Transthoracic echocardiography should be considered in patients with heart failure with reduced ejection fraction (HFrEF) 3–6 months after the start of optimal medical therapy, or if there has been a change in clinical status, to assess the appropriateness for other treatments, including device therapy (implantable cardioverter defibrillator [ICD] or cardiac resynchronisation therapy [CRT], or both).
* BNP and NT proBNP levels may be considered in patients with an established diagnosis of heart failure for prognostic stratification.
35
Acute heart failure: Recommendations for investigations and management:
1. Investigation and management of precipitating factors is recommended in all patients presenting with acute heart failure. Acute coronary syndrome (ACS), hypertensive crisis, arrhythmia, mechanical catastrophe (e.g., ruptured interventricular septum, mitral papillary muscle or LV free wall, or acute valvular regurgitation), and pulmonary embolism should be confirmed or excluded, and managed immediately
2. Monitoring of peripheral arterial oxygen saturation
3. oxygen therpay recommended in patiend with 02 less than 94%
4. non-invasive ventilation should be considered in all patients with acute pulmonary oedema/congestion who remain Hypoxaemic and tachypnoeic despite oxygen therapy to improve symptoms and requirement for intubation
5. IV loop diuretics asre recommended- assist with congestion and improve symptoms of fluid overload
6. IV vasodilators may be considered in patients with systolic BP more than 90mgHg to relieve symptoms
7. Intravenous iontropic therapy: Consider in all pts with signs of peripheral hypoperfusion (usually with systolic BP \<90mmHg) and congestion refractory to other treatments- to overall improve end organ dysfunction
36
Pharmological management of chronic heart failure:
What medications and benefits associated with each?
ACE inhibitors
* An ACE inhibitor is recommended in all patients with HFrEF associated with a moderate or severe reduction in LVEF (LVEF less than or equal to 40%) unless contraindicated or not tolerated to decrease mortality and decrease hospitalisation
* An ACE inhibitor may be considered in patients with HFrEF associated with a mild reduction in LVEF (LVEF 41–49%) unless contraindicated or not tolerated to decrease mortality and decrease hospitalisation.
Beta blockers
* A beta blockera is recommended in all patients with HFrEF associated with a moderate or severe reduction in LVEF (LVEF less than or equal to 40%) unless contraindicated or not tolerated, and once stabilised with no or minimal clinical congestion on physical examination to decrease mortality and decrease hospitalisation.
* Specifically, bisoprolol, carvedilol, metoprolol (controlled release or extended release) or nebivolol
* Beta blocker may be considered in patients with HFrEF associated with mild reduction in LVEF- 41-49%
MRAs: (mineralocorticoid antagonists)
* An MRA is recommended in all patients with HFrEF associated with a moderate or severe reduction in LVEF (LVEF less than or equal to 40%) unless contraindicated or not tolerated, to decrease mortality and decrease hospitalisation for heart failure
* MRA may be considered in patients with HFrEF associated with a mild reduction in LVEF (LVEF 41–49%) unless contraindicated or not tolerated, to decrease mortality and decrease hospitalisation for heart failure
Diuretics (Loop diuretics)
* A diuretic should be considered in patients with heart failure and clinical symptoms, or signs of congestion, to improve symptoms and manage congestion.
Angiotensin receptor blockers (ARBs)
* An ARB is recommended in patients with HFrEF associated with a moderate or severe reduction in LVEF (LVEF less than or equal to 40%) if an ACE inhibitor is contraindicated or not tolerated, to decrease the combined endpoint of cardiovascular mortality and hospitalisation for heart failure.
* An ARB may be conisdered in patients with HFrEF associated with a mild reduction in LVEF (LVEF 41–49%) if an ACE inhibitor is contraindicated or not tolerated, to decrease the combined endpoint of cardiovascular mortality and hospitalisation for heart failure.
ARNI: Angiotensin receptor neprolysin inhibitor:
Angiotensin receptor neprilysin inhibitor (ARNI)
* An ARNI is recommended as a replacement for an ACE inhibitor (with at least a 36-hour washout window) or an ARB in patients with HFrEF associated with an LVEF of less than or equal to 40% despite receiving maximally tolerated or target doses of an ACE inhibitor (or ARB) and a beta blocker (unless contraindicated), with or without an MRA, to decrease mortality and decrease hospitalisation.Strong
* **Concomitant use of ACE inhibitors and ARNIs are contraindicated and these medications should not be administered within 36hours of each other, because of an increased risk of angioedema.**
Ivabradine
* Ivabradine should be considered in patients with HFrEF associated with an LVEF of less than or equal to 35% and a sinus rate of 70 beats per minute (bpm) and above, despite receiving maximally tolerated or target doses of an ACE inhibitor (or ARB) and a beta blocker (unless contraindicated), with or without an MRA, to decrease the combined endpoint of cardiovascular mortality and hospitalisation for heart failure
Hydralazine plus nitrates:
* Hydralazine plus nitrates may be considered in patients with HFrEF if an ACE inhibitor and ARB are contraindicated or not tolerated to decrease mortality.Weak
* Hydralazine plus nitrates may be considered in black patients of African descent with HFrEF despite receiving maximally tolerated or target doses of an ACE inhibitor (or ARB) and a beta blocker (unless contraindicated), with or without an MRA, to decrease mortality and hospitalisation for heart failure.
Digoxin:
* Digoxin may be considered in patients with HFrEF associated with sinus rhythm and moderate to severe symptoms (New York Heart Association [NYHA] Class 3–4) despite receiving maximally tolerated or target doses of an ACE inhibitor (or ARB) to decrease hospitalisation for heart failure
37
What are non drug interventions for heart failure? (think education)SNAP
38
What is the Indication, MOA, Adverse effects, and precautions to be taken with the following medications
ACE inhibitors
Angiotensin receptor antagonists (Sartans)
39
What is the indication, MOA, adverse effects and precautions for the following medications?
Beta blockers
40
Indication, Mechanism of action, side effects, precautions:
Aldosterone antagonists?
Sacubitril with valsartan?
41
Indication, Mechanism of action, side effects, precautions:
Diuretics
Ivabradine
42
Indications, Mechanism, side effects, precautions for the following:
Digoxin (HF)
43
What role do implantable devices play in HF? (e.g defib,)
44
What drugs should be avoided in heart failure?
45
Take home messages when managing HF - just read
46
What is the NYHA classification for HF? (Outline the 4 stages and associated features) (pt symptoms)
47
What is the definition of heart failure?
How can is it defined in terms of LVEF?
48
What are most common causes of heart failue (aetiology)
49
What is the pathophysiology of HF?
50
What is the framingham criteria for the diagnosis of CHF?
51
Case examples: and other presentations- just read.
52
What needs to be covered in patient history - HF?
53
Physical examination findings for HF
Important investigations?
54
Key diagnostic features in heart failure? (clinical features)
55
Risk factors HF? (list 6)
56
1st line investigation to order in heart failure?
Think bedside, Bloods, Imaging.
What other investigations can be considered?
57
Differentials for Heart failure?
58
What are the general principles of management for heart failure?
59
When would ICD and CRT be indicated for heart failure? (know briefly)
60
Treatment alogrihtm for Heart failure:
61
Lifestyle modifications for heart failure?
62
What are the key primary prevention strategies for heart failure?
63
What should be discussed for patients with heart failure? (on discharge/GP settings) OSCE
64
What role does training and rehab have in heart failure?
65
Complications of heart failure? (list 6)
66
Valvular heart disease:
Know:
4 different valve patholgies:
67
Mitral regurgitation (MR)
What is it?
Causes?
Symptoms?
Exam findings?
Investigations:
Management?
Backflow through mitral valve in systole
Acute
* Acute MI (most common)
* Other causes of papillary muscle rupture (trauma, surgery etc.)
* Infective endocarditis (causes all types of regurgitation murmurs)
**Chronic**
* Mitral prolapse (congenital)
* RHD
* LV dilation (CHG, DCM, aneurysm)
* Marfan's
Symptoms:
* Same as CHF (dyspnoea, fatigue,palpitations)
Signs/Exam findings:
* Pulse: AF, sharp upstoke (rapid LVdecompression)
* Resp: bibasilar creps
* Palpation: displaced and thrusting (hyperdynamic) apical pulse (similair to AR) apical thrill
* pansystolic murmur - radiating to axilla!
* Heard best at apex; Valsalva manoeuvre- S3 later
Investigations:
* ECG: LVH, LA enlargement
* CXR: LVH, LA enlargement, CHF findings
* Echo: to assess LV function, and MR severity and assess for repair/ valve replacement surgery
Management:
* Asymptomatic: monitor with serial echos
* Medical: ACEi to reduce afterload, and diuretics (decrease preload)
* Treat concominant AF- rate+anticoagulate
* Surgery: Indications- (valve repair or replacement) Acute MR, papillary muscle ruputre, NYHA III-IV CHF, AF, worsening LVfunction
68
Mitral stenosis:
Eitology:
Symptoms
Signs/Exam:
Ausculatation?
Investigations and findings: (ECG, CXR, ECHO)
Management:
* Avoid exertion
* Manage AF and CHF
* Anticoagulate if AF/ atrial thrombus
* Benzylpenicillin IM if RHD
* Surgery- CHF (class II-IV), failure of medical therapy
Eitology: RHD!, congential (rare)
Symptoms: Signs of CHF, MITRAL facies (insufficent CO- facial flushing)
Signs/ Exam:
* General - mitral facies, cyanosis, CHF signs
* RR - tachypnoea
* Pulse - AF (major complication)
* JVP - normal unless RSHF
* Resp - bibasilar creps
* Carotid - reduced volume
* Palpation - tapping apex beat, palpable diastolic thrill at apex
Auscultation:
* **Loud S1**
* **Opening snap of mitral valve**
* Low pitched rumbling mid diastolic murmur
* Heard best: Apex, left lateral with bell after exertion (ask to sit up and down in bed a few times)
Investigations:
* ECG: AF, LA enlargement (p mitrale), RVH (congestion)
* CXR: LA enlargement (↑carinal angle, extra bump along upper L heart border, double R heart border), CHF
* Echo: MS
Management:
* Avoid exertion
* Manage AF and CHF
* Anticoagulate if AF/ atrial thrombus
* Benzylpenicillin IM if RHD
* Surgery- CHF (class II-IV), failure of medical therapy
69
Aortic Stenosis:
Aetiology:
Symptoms:
Exam/Signs:
Auscultation:
Investigations:
Management:
Aetiology:
* Bicuspid aortic valve (young)
* **Aortic calcific degeneration (elderly)**
* RHD (usually with AR)
Symptoms: (triad- Sx triad:
1. Angina (LV hypertrophy, decreased diastolic pressure)
2. Syncope
3. SOBOE
4. Others: PND, orthopnoea, edema
Exams/Signs:
* Vitals - tachycardia, narrow pulse pressure (less blood into aorta), tachypnoea
* Carotid - slow rising plateau pulse, auscultate to rule out carotid stenosis
* Palpation - displaced and sustained (↑ejection time) apical impulse, systolic thrill
Auscultation:
* Systolic ejection murmur
* Cresendo-decrescendo
* Radiates to carotid
* May have ejection click
* Soft S2
* S4 (LVH/pressure overload)
* May have AR
* **Heard best - over aortic area, sitting forward with breath held on deep expiration**
Investigations:
* ECG - LAD, LVH, LBBB, AF
* Echo -↓valve area, LVH, ↓LV function
* CXR - post-stenotic aortic dilation, calcified valve, LVH, LA enlargement, CHF late
Management:
* Asymptomatic - monitor with serial echo's yearly
* Medical (not surgical candidates or temporary while waiting for surgery)
* Mild activity only
* Optimise RFs (statin, DM, HTN)
* Avoid nitrates, B-blockers & other vasodilators even with angina (↓BP)
* Manage heart failure with ACEi and diuretics
* Surgical - AV replacement is indicated for symptomatic AS (only effective therapy)
70
Aortic regurgitation:
Aetiology:
Symptoms:
Examination/Signs:
Auscultation:
Investigations:
Management:
* Bicuspid aortic valve
* Infective endocarditis
* RHD
* Aortic dissection
* Marfan's syndrome
* Syphilitic aortitis
Symptoms:
* LVH compensation means AR often remains asymptomatic for decades
* Late stage become symptomatic - signs of LV failure + angina
Exam (important in AR)
* General - Marfan's stigmata
* Vitals - wide pulse pressure, tachycardia/tachypnoea
* Pulses - bounding carotid pulsations, rapid upstroke with collapsing downstroke, collapsing best assessed with radial pulse held above head
* Palpation - displaced and hyperdynamic/heaving , thrill
Auscultation:
* Early diastolic decrescendo murmur
* Heard best - left sternal border, lean forward on deep expiration
* S3 in severe LV failure
Investigations:
* ECG: LVH, LAD, LA enlargement
* CXR: cardiomegaly, LA enlargement, aortic root dilation
* Echo: AR
* Exercise testing: become hypotensive
Management: Process
* Asymptomatic: monitor with serial echos in long asymptomatic phase
* Symptomatic: avoid excessive exertion, treat CHF
* Surgery (AV replacement): if class III or IV NYHA CHF; if LV dilation or LVEF \<50% (regardless of symptomatic or not)
* If not surgical candidates manage as for CHF (ACEi, B-blocker, diuretics)
71
TR?
TS?
PR?
PS?
Mitral valve prolapse?
(Signs/symptoms) + Auscultation, Investigation findings?
72
Dynamic Manoeurvres and systolic cardiac murmurs:
73
Aortic stenosis:
Pathophysiology (age relate)
Risk factors?
Complications?
74
Aortic regurgitation:
Pathophysiology: and implications
75
Mitral stenosis:
Pathophysiology:
76
Mitral regurgitation:
Patho:
Mitral valve prolapse:
Eitology:
Pathology:
Marfans syndrome:
Eitology:
Clinical/Examination:
Complications:
77
Libman-sacks endocarditiis:
Carcinoid heart disease:
Right sided valve disorders:
Valve repair and replacement:
78
Infective endocarditis:
Pathology:
Frequency of valve involvement?
Risk factors?
Microbial eitiology: ? List 4-6 common organism
Pathophysiology:
79
**Infective endocarditis:**
Clinical features: for: Acute and subacute endocarditis
Typical presentation: (symptoms/signs)?
Examination findings?
Complications?
DDX?
80
How is bacterial endocarditis diagnosed? (what is the Dukes modified criteria) list.
Investigations and findings?
Management? (non-pharm, medical management, surgical, ongoing investigations, supportive?
81
What is non-bacterial thrombotic endocarditis? (NBTE)
What role does prosthetic valves have in bacterial endocarditis? What are pros vs cons of them?
82
ARF and RHD:
Epidemiology:
Eitology:
Social risk factors?
Pathogenesis of ARF and RHD?
83
RHD:
Gross morphology?
Micro:?
Valves affected?
84
ARF:
Clinical features in children (0-15yrs), Constitutional symptoms? Cardinal features (systems in ARF)
Investigations+findings?
What is the modified Jones criteria? (JONES CAFE PAL) (Major/minor)
85
What are key questions you need to ask when taking a history and suspecting ARF? Think DDX - e.g swollen joint: septic arthritis, reactive arthritis, ARF monoarthritis
Examination?
Signs/Symptoms?
Complications of ARF?
Complications of RHD?
86
Management of ARF/RHD?
Acute: Non-pharm, medical, supportive, ongoing monitoring, communication (referral, safety net, follow up)
87
Types of Shock? Give examples of each - e.g hypovolemic, distributive)
What are the stages of shock? (compensated, decompensated, irreversible)
What is the definition of organ failure for the various organ systems (e.g renal, CV, Resp, CNS, Liver)
88
What examination findings would you expect from the different classes of shock?
Give a general outline for assessment of shock: (examination of shock)
What are the first line investigations (broadly) you would undertake in a patient with shock? (unknown cause)
89
What is sepsis? When should it be suspected? (what paraemters)
What are signs of sepsis?
What are signs of septic SHOCK?
Infection confirmed or suspected plus:
* Temperature \> 38.3C or \< 36C (normal temperature does not exclude sepsis)
* Respiratory rate \> 20 / minute
* Heart rate \> 90/minute
* Acute confusion or decreased level of consciousness
* Hyperglycemia (blood glucose \> 7.7 mmol/L in patient without diabetes)
* Oliguria (urine output less than 0.5 mL/kg/hour)
Septic shock:
SIGNS SUGGESTIVE OF SEPTIC SHOCK
Infection confirmed or suspected plus:
* Mottled or cold peripheries
* Capillary refill time \> 3seconds
* Systolic BP \< 90 mmHg or MAP \< 60 mmHg
* Purpuric rash
* Arterial or venous lactate \> 2 mmol/L
* Oliguria (urine output less than 0.5 mL/kg/hour
90
What is the general management of sepsis (5 marks)
91
What are sepsis 3 definitions?
What is SOFA score? What is qSOFA (what is measured)
What is septic shock?
What is SIRS? What is the criteria for SIRS?
92
SOFA score (ICU scoring system) for sepsis:
What is pathophysiology of SIRS?
93
Outline a clinical assessment of critical ill patient with sepsis:
Hx
Exam
Investigation: Bedside, labs, imaging, samples (3- 4 marks)
What is the Septic 6 bundle (3 marks outline) (V important)
94
Outline assessment + management of patient with sepsis:
(Primary survery, active management, supportive, ongoing investigations, monitoring and safety netting) (8-10marks)
95
Hypovolemic shock
Haemorrhagic vs fluid loss
What are different 4 satges of haemorrhagic SHOCK?
Where and what systems/patholgies cause fluid loss?
What are general management prinicples of hypovolemic shock? (General measures)
96
What are general management principles for shock (ABCDE\_ list - 5marks
Specific conditions:
Anaphylaxis management?
Sepsis?
Haemorrhagic shock?
Management
General measures
* A - secure if required
* B - high flow O2; monitor for \>93%
* C
1. IV access with 2 large bore (14 or 16 gauge) cannula in antecubital veins
2. Immediate IVF replacement with Nsaline (titrate until JVP ~3cm above the sternal angle)
3. Omit fluids if JVP already raised or if pulmonary edema present
4. Give cross matched blood aiming for Hb \>70
5. Inotropes - maintain MAP ≥65
97
What are the compensation mechanisms in shock?
What are the fluid distribution in the body?
98
What is Pericarditis?
What are the causes? (idiopathic/infective/non-infective)
Epidemiology:
Clinical features?
DDX?
Physical examination?
Investigations: ECG, Bloods, CXR, ECHO?
99
What are the ECG findings in pericarditis?
Acute?
Evolving?
pericardial effusion?
What is the Management? (3 marks)
Complications? (2 marks)
100
What is constrictive pericarditis?
Eitology:
Clinical features? ( 2.5 marks)
Investigation?
Management prinicples:
How do you differentiate contrictive pericarditis vs cardiac tamponade?
101
What is a Pericardial effusion?
Eitology?
Clinical findings: (2 marks)
Investigations?
Management?
102
Cardiac Tamponade:
Eitology:
Patho:?
Clinical features: Becks, VS, CHF signs (3 marks),
What is Becks triad?
Diagnosis? Investigations?
Management?
103
What is the definition of Primary myocardial disease:
What are the 3 major types?
What is the mechanism of each?
104
What is DCM? Dilated cardiomyopathy:
Pathogenesis:
Common eitologies: List 4-6 (2-3 marks)
How does it present clinically?
Investigations?
Management:
Presentations
* CHF
* Dyspnoea, fatigue, poor exertional capacity, orthopnoea, paroxysmal nocturnal dyspnoea, JVP, pulmonary HTN, edema
* Murmurs - S3, mitral regurgitation
* Arrythmias
* Systemic or pulmonary emboli
* Sudden cardiac death
Ix
* Bloods - FBC, UECs, LFTs, BNP, troponin, CK, TSH, iron studies
* ECG - arrhythmias, ST-T wave abnormalities, BBB, poor R wave progression
* CXR - cardiomegaly (globular), signs of CHF
* Echo - ↓LVEF (systolic impairment), hypokineisa (global), chamber enlargement, MR & TR, mural thrombi
Management
* Immunise - influenzae, S.pneumoniae
* Treat underlying cause e.g. abstinence from alcohol
* Treat HF
* Treat arrhythmias
* Anticoagulation - warfarin for those with AF, thromboembolism history, documented thrombus
* Surgical - transplant for severe disease
105
Myocarditis:
Eitology: Infectious (Viral, Bacterial, parasite,fungal)
Clinical findings: 2 marks
Investigations+findings:
Management:
106
Hypertrophic cardiomyopathy:
Eitology:
Patho:
Pathology:
Clinical features (list 6 ) 3 Marks
Complications?
Investigations?
Management?
107
Restrictive Cardiomyopathy:
What are the major causes: List 4 (2 marks)
Pathogenesis?
Pathology:
Clinical features: List 2
Investigations?
Management:
108
What is an Aneurysm?
What is a true Aneurysm? False Aneurysm?
Aortic Aneurysm: Causes? (List 5-6)
Micscopic findings?
Risk factors?
109
Clinical Features: (triad) AAA features?
TAA clinical features?
Management?
Emergency management?
Complications of aneurysms?
110
Aortic dissections:
Overview:
What is the stanford classification \*type A, type B.
Epidemiology:
Eitopathogenesis?
Pathology:
**Clinical features:**
**Symptoms? Complications?**
**Examination findings:**
**Investigations: +findings**
**Management: ABC+ Medical+surgical**
111
What is Carotid stenosis?
Risk factors?
Clinical?
Ix?
Management?
112
Which vasculitis's effect large, medium and small vessels?
What are the most affected vessels?
What are the different patholgical mechanisms by which they are defined? (E.g Immune complex mediated, ANCA+, Anti-endothelial abs, infectious vasculitis
113
What is Giant cell (temporal) arteritis?
Pathology: Gross/Micro?
Patho?
Features/Signs?
Associations?
Treatment?
114
What is Giant cell (temporal) arteritis?
Pathology: Gross/Micro?
Patho?
Features/Signs?
Associations?
Treatment?
Prognosis?
V2 - Toronto notes 2021
115
What is Takayasu arteritis? (same patho as GCA?) aka pulseless disease...
116
What is PAN - Polarteritis nodosa? (PAN\*) (Medium/small vessel vasculitis)
What is it? Eitology? (common cause 30%)
Pathology? Organs affected?
Gross/micro:
Clinical features?
Investigations?
Treatment?
117
What is PAN - Polarteritis nodosa? (PAN\*) (Medium/small vessel vasculitis) V2 Toronto notes 22
Defintion
How is it Classified
Eitology+Pathophysiology?
Signs and symptoms?
Investigations?
Treatment:
118
What is Kawasaki's disease? (what is it similair to and who does it affect)?
Microscopy?
Clinical features? (CRASH burn)
Complications?
+ Toronto notes
Diagnositic criteria?
Management?
Complications?
119
What is Granulomatosis with polangitis? (GPA -formerly -Wegners granulomatosis) - Small vessel - ANCA associated
Pathology? Gross/micro
Pathogenesis? (what markers will be positive)
Clinical features?
Diagnosis? (most specific)
Management?
120
GPA- Granulomatosis with polyangitis: Toronto notes:
Defintion:
Classification/Criteria:
Eitology/pathophysiology?
Signs and symptoms?
Investigations?
Treatment?
121
What is Buergers disease? Pathology?
Epidemiology? (MOST common association)
Pathogenesis?
Presentation?
Treatment?
122
What is pyogenic granuloma?
123
What is Kaposi Sarcoma?
What is angiosarcoma?
What is Raynauds disease? What are the types Primary vs secondary? What are the clinical features?
124
Digoxin Toxicity:
How does it occur? E.g mechanism of action? Triad of signs?
Risk factors?
Clinical features? (2 types - acute vs chronic)
Features?
Management? - resus, risk assessment, supportive care, decontamination, antidote?
125
Indications for implanted pacemakers?
What do they consist of? How are they connected?
126
What is an implantable cardioverter-defibrillator (ICD) ?
Mechanism?
Indication?
127
Cardiac Stress testing:
EST:
Indications?
Contraindications- absolute/relative?
Limitations?
Pre-assessment: What to explore HX, exam, ix,
128
How do you establish target HR for Cardiac stress testing? (part of assessment continued)
ECG interpretation
Symptoms?
Indications to cease EST?
Test end points?
Life threatening complications?
Documentation?
129
ECG changes suggestive of ischaemia on EST?
130
Common CV medications:
Know ACEi, ARBs, ARNIs,
131
Common CV medications:
Beta1 Antagonist
Beta 2 Antagonists
CCBs:
SGLT 2 inhibitors
132
CV medications:
Diuretics- types (indications + SEs)
Inotropes: Digoxin!
133
Common Anticoagulants: Types, Moa, Indicatiosn, contraindications, Side effects:
Warfarin:
Heparins:
Direct thrombin inhibitors
Direct factor Xa inhibitors
134
Antiplatelets: Types, Moa, Indicatiosn, contraindications, Side effects:
Thrombolytics
Nitrates:
135
Lipid lowering agents: Types, Moa, Indicatiosn, contraindications, Side effects:
136
