Cardiology Flashcards
What is atherosclerosis
Hardening/narrowing of arteries due to plaque
Clinical Presentation of atherosclerosis
Risk factors of atherosclerosis (7)
Age
Tobacco smoking
High serum cholesterol
Obesity
Diabetes
Hypertension
Family history
Complications of Atherosclerosis
Gangrene
Stroke
Heart attack
Structure of an atherosclerotic plaque
Lipid
Necrotic core
Connective tissue
Fibrous cap
What causes LDL being deposited in atherosclerosis
Endothelial dysfunction
Summarise the main stages involved in the formation of an atherosclerotic plaque
Endothelial dysfunction
1. High LDL deposits in tunica intima. LDL becomes oxidised, activating endothelial cells
- Adhesion of blood leukocytes to activated endothelium moving to tunica intima
- Macrophages take in oxidised LDLs, becoming foam cells
- Foam cells promote the migration of smooth muscle cells from tunica media to the intima and smooth muscle cell proliferation
- Increased smooth muscle cell proliferation and heightened synthesis of collagen
- Foam cells die, causing lipid content released
- Thrombosis plaque ruptures lead to blood coagulation and thrombus impeding blood flow.
Describe the progression of atherosclerosis
1. Fatty streaks
Earliest lesion of atherosclerosis
Appear at a very early age (<10 years)
Consist of aggregations of lipid-laden macrophages and T lymphocytes within the intimal layer of the vessel wall
2. Intermediate lesions
Composed layers of vascular smooth muscle cells, T lymphocytes, adhesion and aggregation of platelets to vessel wall
3. Fibrous plaques of advanced lesions
Impedes blood flow
Prone to rupture
Contains smooth muscle cells, macrophages and foam cells and T lymphocytes
4.Plaque rupture
The fibrous cap has to be resorbed and redeposited in order to be maintained
-if the balance shifts, the cap becomes weak and the plaque ruptures
Thrombus formation and vessel occlusion
What is a limiting factor to treating coronary artery disease?
Restenosis: Drug-eluting stents improve the duration of stents; anti-proliferative and inhibit healing
Useful drugs in treating coronary artery disease
Aspirin – irreversible inhibitor of platelet cyclo-oxygenase
Clopidogrel/ ticagrelor – inhibits of the P2Y12 ADP receptor on platelets
Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis.
Major cell types involved in atherogenesis are …
endothelium, macrophages, smooth muscle cells and platelets
Name the nodal cells
SA node
AV node
AV bundle (Bundle of His)
Bundle branches (L&R)
Purkinje fibers
State the pacemakers of the heart
Sinoatrial node – dominant pacemaker with an intrinsic rate of 60-100bpm
Atrioventricular node – back up pacemaker with an intrinsic rate of 40-60 bpm
Ventricular cells – back up pacemaker with an intrinsic rate of 20-45 bpm
Who sets the sinus rhythm and how many bpm
SA node. 60-100bpm
Action potential from SA node goes to…. and what happens as a result
Bachman’s bundle: Depolarises the LA
Internodal branches: Depolarise RA
The SA bundle sends action potential to the rest of Right atrium via the
Internodal pathway
What does Limb lead 1 show activity of?
High lateral wall of LV
Where does the internodal branch converge?
AV node
What is the importance of AV node
Acts as a gateway between atria and interventricular septum
What is the importance of AV node delay
Want to give time for the atria to contract before the ventricles contract
How is AV node delay created?
Has fewer gap junctions than other nodal cells
Have a smaller diameter (slower conduction speed)
What does Limb lead 2+3 show activity of
Inferior wall of the heart
Cardiac conduction system
- SA node
- AV node
- Bundle of His
- L/R Bundle branches
- Purkinje fibers
What does aVR show activity of?
RV + Basal septum
What does aVL show activity of?
High lateral wall of LV
What does aVF show activity of?
Inferior wall of the heart
Where would you place V1
right 4th intercostal space, parasternal space
Where would you place V2
Left 4th intercostal space (parasternal line)
Where would you place V3
Between V2 + V4
Where would you place V4
left 5th intercostal space, mid clavicular line
Where would you place V5
Left 5th intercostal space, anterior axillary line
Where would you place V6
Left 5th intercostal space, mid axillary line
What is happening to the R wave as you go through V1-V6
Getting bigger
What is happening to the S wave as you go through V1-V6
Getting smaller
What do V1-V3 tell us about the activity?
RV
What limb leads tell us about the right ventricle
V1-V3
aVR
What does V2-V3 tell us about the activity of?
Basal septum
What limb leads tell us about the basal septum
V2-V3
aVR
What limb leads tell us about the anterior wall of the heart
V2-V4
What does V2-V4 tell us about the activity of?
Anterior wall of heart
What does V5-V6 tell us about the activity of?
LV
What limb leads tell us about the LV
V5-V6
Limb lead 1
aVL
How long should PR interval be?
<=0.2 secs
How long should QRS wave be?
<=0.12 secs
What is the Electrocardiogram?
a measure of the currents generated in the EXTRACELLULAR FLUID by the changes co-occurring in many cardiac cells
What is a P Wave?
Atrial depolarisation - seen in every lead apart from aVR
What is the PR Interval?
Time taken for atria to depolarise and electrical activation to get through AV node
What is the QRS complex?
Ventricular depolarisation, still called QRS even if Q and/or S are missing depending on what lead you are looking at
What is the ST Segment?
Interval between depolarisation & repolarisation
What is the T wave?
Ventricular repolarisation
What happens to the ST segment in an Acute Anterolateral Myocardial Infarction?
ST segments are raised in anterior (V3-V4) and lateral (V5-V6) leads
What happens to the ST segment in an Acute Inferior Myocardial infarction?
ST segments are raised in inferior (II, III, aVF) leads
Why is atrial repolarisation usually not evident on an ECG?
since it occurs at the same time as the QRS complex so is hidden
What are the 12 leads on a 12 lead ECG?
Standard limb leads (I, II & III)
Augmented leads (aVR, aVL & aVF)
The precordial leads (V1 - V6)
When reading an ECG, what are the times represented by the small squares and the big squares?
When reading an ECG, the graph shows changes in voltage over time, each small square across represents 40ms & each big square across represents 0.2s
Are P waves positive?
In a normal ECG the p waves are POSITIVE in EVERY LEAD (apart from the aVR)
What is angina?
Chest pain thats felt due to lack of blood flow to the heart muscle
What causes angina?
Reduced blood flow, which causes ischaemia in the heart muscle
Different types of angina?
Stable
Unstable
Prinzmetal’s angina
Which is the most common type of angina
Stable angina
When does stable angina occur?
When the patient has greater than or equal to 70% stenosis (blocked by plaque build up)
When do individuals with stable angina experience chest pain?
During exercise or stress as the heart works harder
The pain goes away with rest
What is the underlying cause of stable angina?
atherosclerosis of one or more coronary artery
What are the other heart conditions that leads to stable angina?
Hypertrophic cardiomyopathy (genetic)- thickened muscle wall so needs more oxygen
Pumping against high pressure
- Aortic Stenosis: narrowing aortic valve
- Hypertension
What is a classic finding of stable angina, and how does this result in angina?
Subendocardial ischaemia causes adenosine & bradykinin release, which stimulates the nerve fibres in the myocardium resulting in the sensation of pain
Where is pain felt in a patient with stable angina
Pressure or squeezing
left arm, jaw, shoulders, back
Alongside pain what else can a patient with stable angina experience
Shortness of breath
Diaphoresis
How long does stable angina last?
20 mins
subsides after exertion or stress taken away
What differentiates stable angina from unstable angina
Stable angina -pain during exercise or stress
Unstable angina - pain during exercise and stress AND rest. It doesn’t go away
How is unstable angina caused ?
Rupture of atherosclerotic plaque with thrombosis
What does a patient with unstable angina classically present
Subendocardial ischaemia
Should be treated as an emergency because patients are at a high risk of progressing to myocardial infarction
What is the key differentiation of angina from myocardial infarction?
Angina: heart tissue is alive but ischaemic
Myocardial infarction: tissue has begun to necrose
What do patients with vasospastic (Prinzmetals) angina also present/nor present with
May or may not have atherosclerosis.
Ischaemia from coronary artery vasospasms: when the smooth muscle around the arteries constricts extremely tightly and reduces blood flow enough to cause ischaemia
When does a patient with vasospastic angina feel pain
Anytime
What is a classic presentation of patients with vasospastic (Prinzmetals) angina
Transmural ischaemia: Entire thickness of myocardium
Table explaining simarilities/differences of angina
Also in stable and unstable angina the no of cardiac markers (troponin) are not elevated
Risk Factors for angina
Investigations for angina
FBC
EUC
Blood glucose levels
Lipid Profile
Chest X-ray
Test to induce ischaemic chest pain
Exercise ECG
Stress echocardiography
Myocardial perfusion scanning
Management for angina
Non-pharmacological
Education
Smoking cessation
Alcohol limitation
Lose weight
Exercise
Healthy diet
Pharmacological (BANS)
Beta-blockers (calcium channel blockers if contraindicated)
Aspirin
Nitrates
Statins
Complications for angina
Acute Coronary Syndrome
What is Acute Coronary Syndrome
Reduction/loss or total occlusion of blood supply to the heart muscle
Clinical symptoms of Acute Coronary Syndrome
Retrosternal Pain (for at least 30min), which radiates to the neck, arms and jaw. The pain is described as crushing, heavy or like a tight band. Worse with physical or emotional exertion. It is not relieved by rest. Nitrate spray (within a couple of minutes) may not always relieve the pain. The acute coronary syndrome may accompany diaphoresis, a feeling of impending doom and breathlessness.
Remember, Patients classically clinch their fist and hold it on their chest to describe the pain (Levine’s Sign)
Examination
Signs of impaired myocardium
Hypotension, Oligouria
Raised JVP
Narrow pulse pressure
Third heart sound
Lung crepitation (pulmonary oedema)
Is Acute Coronary syndrome considered a medical emergency ?
Yes
What is a non STEMI
MI, but without ST-segment elevation. May have other ECG changes, such as ST-segment depression or T-wave inversion. Will have elevated cardiac biomarkers.
The coronary artery is only partially occluded causing infarction
As a result of Ischaemia proximally : the infarction of the myocardial tissue occurs proximally to where that vessel supplies.
What are the risk factors of developing acute coronary syndrome
What is STEMI
MI is an acute myocardial infarction with ST-segment elevation of more than 0.1 mV in two or more contiguous leads and elevated cardiac biomarkers.
Complete occlusion of the coronary artery causing infarction
What causes myocardial infarction?
Death of cardiomyocytes distally and then slowly progress proximally unless resolved
Results in no oxygen going to the heart muscle in that area
Causes of chest pain by body systems
Why do you see an increase in cardiac serum markers within blood ? and what day do these levels peak following myocardial infarction
When cardiac muscle cell dies the troponin and ck-mb get released into circulation
Troponin peak: day 2
CK-mb peak : less than day 2
Why is measuring troponin levels important?
useful and important in diagnosing STEMI and NSTEMI
What do we refer to as acute coronary syndrome
STEMI
Non STEMI
Unstable angina
Investigations for Acute Coronary Syndrome
Chest pain with high suspicion of Acute Coronary syndrome (history, examination and risk factors)
ECG - tall T-wave, ST elevation or new Left Bundle Brach Block
FBC
EUC
Glucose
Lipid profile
Cardiac Enzymes
Troponin T (cTNT) and Troponin (cTNl) are proteins virtually exclusive to cardiac myocytes. They are highly specific and sensitive, but are only maximally accurate after 12 hours.
Creatinine Kinase - CK-MM, CK-BB, CK-MB
Think Don’t be fooled by normal cardiac enzymes. A fresh MI (< 30 minutes) may not yet show elevated blood levels.
Remember Troponin can be released into blood when cardiac muscle is damaged by pericarditis, PE with a large clot or sepsis. Renal failure also reduces the rate of troponin excretion.
Diagnosis of acute coronary syndrome
Diagnosis (at least two of the following):
Typical chest pain persisting for more than 30 minutes
Typical ECG findings
ST elevation
Pathological Q wave
Elevated cardiac biomarker levels.
Troponin (peaks in 1 -2 days) lasts 2 weeks
CK-MB - rises 4-6 hours peaks at 12 and at 2 days drops off
ECG changes within acute coronary syndrome
ECG is an important investigation tool for the identification and diagnosis of ACS and other cardiovascular diseases. Record ECG as soon as possible in suspected MI. Look at ST segment and look for:
ST elevation
ST depression
ST Elevation Infarction of cardiac muscles results in ECG changes that evolve over hours, days and weeks in relatively predictable fashion.
Location of myocardial infarction can be identified with the ECG leads.
Location of Infarct ST elevation in leads
Anterior V2-V5
Antero-lateral I, aVL, V5, V6
Inferior III, aVF (sometimes II also)
Posterior
Right ventricular
Remember The deeper the q- wave the longer the infarction has been.
Where does myocardial infarction tend to occur?
1.LAD
2.RCA
3.LCX
If left untreated what can unstable angina lead to?
Non STEMI: significant occlusion of artery becasue of a ruptured plaque, subsequent thrombosis leading to poor oxygen supply.
However the artery is NOT fully occluded
Describe an NSTEMI regarding ischaemia and infarction
Infarction distally
Ischaemia proximally
To artery supply
Leads to subendocardial infarction
What can a NSTEMI progress to?
STEMI: significant occlusion of artery becasue of a ruptured plaque, subsequent thrombosis leading to no oxygen supply.
** Artery is fully occluded**
Describe a STEMI regarding ischaemia and infarction
Infarction distally & Infarction proximaly to the artery supply
Leads to transmural infarction
What does New LBBB regarding STEMI suggest?
Infarction of the septum of the heart where the left bundle branch goes through
Pathophysiology of acute coronary syndrome
Describe the presence of cardiac markers in:
Unstable angina
NSTEMI
STEMI
Unstable Angina: No increase
NSTEMI & STEMI: Increase
Management of Acute Coronary Syndrome
Must consider the following in managing ACS:
The suspicion of acute MI based on the clinical and ECG findings
Deciding whether the patient has indications or contraindications for thrombolytics or primary percutaneous coronary intervention
It excludes other diagnoses that might mimic acute MI but would not benefit from or might be worsened by anticoagulation or thrombolysis (eg, acute pericarditis, aortic dissection).
Acute management
Admission to the coronary care unit
Explain to the patient what has happened
Morphine
Oxygen
Nitrates
Aspirin
Clopidogrel
Acute management Reperfusion therapy
Percutaneous coronary intervention (PCI) OR Fibrinolytic therapy (thrombolysis)
Remember MONAC Morphine (+/- antiemetic), Oxygen, Nitrates, Aspirin, Clopidogrel
Acute management Reperfusion therapy
Early reperfusion with PCI or thrombolytics reduces mortality, preserves ventricular function in patients with ST-segment elevation, has no contraindications, and receives treatment within the first 6 to 12 hours.
PCI should be performed within the:
60min if a patient presents within the first hour of symptom onset
90min if patient presents between 1-3hrs after symptom onset
90 to 120 minutes for patients presenting between 3 and 12 hours
If these targets cannot be reached, fibrinolysis should be given within 30 minutes of arrival at the hospital
Fibrinolytic therapy (Thrombolysis) within 24 hours, contraindication > 24 hours
Alteplase OR
Reteplase
Anticoagulant therapy
Heparin
Heart Bypass
Indications for reperfusion therapy
Ischaemic/infarction symptoms of longer than 20 minutes (chest pain-radiating to shoulder or jaw, to sweat, feeling of doom
Symptoms commenced within 12 hours
ST elevation or presumed new left bundle branch block on ECG
No contraindications to reperfusion therapy.
Pharmacology Thrombolytics break down/dissolve clots. It is used to treat stroke, pulmonary embolism and myocardial infarction. Three main thrombolytic drugs: tissue plasminogen activator, streptokinase, and urokinase. Side effects: major bleeding, cardiac arrhythmias, cholesterol embolus syndrome, anaphylactoid reaction, cerebrovascular accident, intracranial haemorrhage. Streptokinase-specific adverse effects: Non-cardiogenic pulmonary oedema, hypotension, fever and shivering.
Contraindications and cautions for thrombolysis use in STEMI
Risk of Bleeding (active bleeding, haemorrhage ophthalmic condition, known bleeding diathesis, suspected aortic dissection)
Risk of intracranial haemorrhage
Recent Major trauma, surgery, head injury < 3 weeks
Aortic Dissection
Pregnancy
On-going management Non-pharmacological
Smoking cessation
Alcohol limitation
Diet modification
Lose weight
On-going management pharmacological (ABAS)
ACE inhibitors OR Angiotensin Receptor Blocker
Beta-blockers
Aspirin + clopidogrel
Statins
Long-term anticoagulation to prevent emboli from left ventricular mural thrombus should be considered in patients who have suffered a large myocardial infarction, particularly if a large akinetic/dyskinetic area is present.
Pharmacology Aspirin is a COX 1/2 inhibitor. It prevents the production of Prostaglandins (inflammation: fever and pain) and thromboxane (clotting). It is used to treat fever, osteoarthritis, heart conditions and stroke. Side effects: nausea/vomiting, dyspepsia, stomach ulcer or bleeding problems, headache, dizziness, tinnitus, renal dysfunction and Reye’s syndrome (particularly in children who have taken aspirin)
Pathology of Acute Coronary Syndrome
Type of infarct
Transmural
It affects all of the myocardial wall
ST elevation and Q waves
Subendocardial
Necrosis of <50% of the myocardial wall
ST depression
Think: ST-segment elevation on ECG indicates that the infarction extends through the full thickness of the myocardial wall (transmural). The absence of ST-segment elevation in the setting of cardiac enzymes indicates that the infarction is limited to the subendocardium. NSTEMIs are dangerous in that the patient is still at risk for a full-thickness infarct in that area
Complications of acute coronary Syndrome
Complication
Arrythmia
Myocardial Rupture
Shock/CHF
Post-Infart Angina
Recurrent MI
Thromboembolism/PE
Pericarditis
Dressler’s Syndrome
Dressler’s Syndrome This is a type of pericarditis that can develops 2-10 weeks after an MI, heart surgery (or even pacemaker insertion).
What is heart failure?
Used to describe an point at which the heart cant supply enough blood to meet the bodys demands
How does heart failure occur?
2 ways:
Systolic Heart Failure: can’t pump hard enough
Diastolic Heart Failure: cant fill enough
=Blood in lungs -> congestion fluid build up
What is systolic heart failure?
When the heart cannot pump hard enough
The ejection fraction is below 40% due to Stroke Volume decreasing
What is ejection fraction?
Stroke Volume/Total Vol
Normal: 50%-70%
Borderline: 40%-50%
Systemic Heart Failure: >40%
What is Diastolic Heart Failure?
The heart cannot fill with enough blood
Low Stroke Volume but Normal Ejection Fraction. Due to reduced preload
What is an important relationship between systolic and diastolic function?
Frank Starling mechanism
What is the Frank Starling mechanism
Shows how loading up the ventricle with blood during diastole and stretching out the cardiac muscle makes it contract with more force.
This increases Stroke Volume during systole
Pathophysiology of heart failre
Classification of heart Failure
What are heart failure cells called
Haemosiderin-Laden macrophages
Left vs Right heart Failure
CVP = Central Venous Pressure
PAP= Pulmonary Arteriole Pressure
Diastolic vs Systolic heart failre
Diagnosis of heart Failure
Primarily a clinical diagnosis
- History
- Physical exam:
bilateral lung crackles
peripheral pitting oedema
rasised JVP
Additional heart sounds: S3 dilation, S4 poor LV compliance - Lab markers
NtproBNP
-Prognostic: 22.5% mortality if >5000pg/ml - Imaging: Chest x ray, echocardiogram
Treatment of heart failure
Preload: diuretics
Afterload: ARBs/ACEi & BB
Neurohorm
Inotrope: norepinephrine/dopamine
Contractility
Device
Rhythm
Anticoagulation/antiplatelet
Iron Studies
Risk reduction
What is cor pulmonale
Abnormal enlargement of the right side of the heart as a result of disease of the lungs or pulmonary blood vessels
Risk Factors for developing cor pulmonale
- Smoking
- Hypercoagulable states
- Hypertension
- Illicit drugs e.g. cocaine abuse
- Valvular heart disease
- Genetics
- Age
- Gender
- Renal insufficiency
- LV hypertrophy
- Dyslipidaemia
Pathophysiology for cor pulmonale
Underlying lung condition causes hypoxia-induced vasoconstriction.
∴ ↑ ↑ Resistance of the pulmonary vessels
∴ Pulmonary hypertension
∴ Harder for RV to pump blood into pulmonary vessels
If ACUTE, rapid rise in pressure ∴ RV stretch out
If CHRONIC, prolonged high pressure ∴ RV hypertrophy
RV hypertrophy -> ↑ Heart muscle ∴ ↓ RV space ∴ ↓ Space for blood to fill
= DIASTOLIC FAILURE
Also, coronary arteries are squeezed by extra muscle
∴ ↓ Less blood delivered to muscle
∴ ↑ Demand & ↓ Supply = RV ischaemia ∴ Weaker contractions
= SYSTOLIC FAILURE
Clinical Manifestations of cor pulmonale
Investigations for cor pulmonale
Differential diagnosis for cor pulmonale
COPD
Pneumonia
Pulmonary embolism
Left-sided Heart Failure, blood gets backed up into ____
Right-sided Heart Failure, blood gets backed up into ____
Lungs
Body
Management of cor pulmonale
Supplemental oxygen (helps w/ hypoxia-induced vasoconstriction) - treats the underlying lung disease
Loop diuretic - reduces oedema from heart failure ∴ and relieves dyspnoea
Lifestyle changes - low salt intake, exercise, stop smoking etc
//
For resistant Cor Pulmonale, heart-lung transplant is possible.
complications of Right-Sided Heart Failure
Congestion in systemic circulation:
Systemic Vein congestion -> Jugular vein distention
Backs up to Liver & Spleen:
Hepatosplenomegaly
Cardiac Cirrhosis & Liver Failure
Ascites
Backs up to leg:
Pitting Oedema
Complications for cor pulmonale
RV failure
Liver dysfunction
Treatment for Right Sided Heart Failure
ACEi
Diuretics
Heart Failure causes a…
arrhythmia: Ventricles out of sync
Signs and symptoms of heart failure (6)
Treatment for Diastolic Heart Failure
Cardiac resynchronisation therapy with patients suffering from arrhythmia
Ventricular Assist Device
End Stage Heart Failure -> Heart Transplant
Treatment for Systolic Heart Failure
Cardiac resynchronisation therapy with patients suffering from arrhythmia
Ventricular Assist Device
End Stage Heart Failure -> Heart Transplant
Are the majority of people with Abdominal Aortic aneurysm symptomatic or asymptomatic?
Asymptomatic
It is often an incidental finding -> Needs monitoring
Where do Abdominal Aortic aneurysm start
90% Below renal artery
15% Extend to common iliac artery
What is an aneurysm
an artery that has enlarged to greater than 1.5 times the expected diameter
What is an abdominal aortic aneurysm (Triple A)
Defined as an aneurysm greater than 5.5cm
Requires treatment
What can an AAA progress to?
ruptured AAA
Anteriorly rupture into peritoneal cavity -> Fatal
Posteriorly rupture into retroperitoneal -> transiently stable
Clinical presentation of AAA
Classical Presentation
Enlarging, painful, palpable, pulsatile, abdominal mass
Potentially, reduced lower limb pulses, distal limb ischemia and/or vascular bruits audible on auscultation
Asymptomatic – 75%
Incidental finding or on routine physical examination, AXR or abdominal ultrasound
Consider for treatment or surveillance
Symptomatic
Pain in central abdomen, back, loin, iliac fossa or groin
Thrombus in aneurysmal sac may be a source of emboli to lower limbs
Inflammation and compression of surrounding structure – ureter or IVC
Rupture
Usually into retroperitoneum
Remember 75% patients with ruptured AAA do not make it to hospital
What is the prognosis of anterior AAA rupture
Poorer prognosis than posteriorly
Differential diagnosis of AAA
Acute Pancreatitis
Mesenteric Ischaemia
Ruptured gastrointestinal ulcer
Appendicitis
Gallstone Disease
Nephrolithiasis
Irritable Bowel Syndrome
Complications of AAA
AAA rupture
Death
Renal Failure
Lower limb ischaemia
Mesenteric ischaemia
Investigations for AAA
Abdominal ultrasound (definitive test)
ESR/CRP
FBC
CT
MRI
Management for AAA
Management of AAA is prevention
Surveillance
Cardiovascular risk reduction - smoking cessation, lose weight
Elective surgical repair - Endovascular Aneurysm Repair
Indications for AAA repair
Male with AAA >5.5 cm
Female with AAA >5.0 cm
Rapid growth >1.0 cm/year
Symptomatic AAA (abdominal/back pain/tenderness, distal embolisation)
Ruptured AAA management
Overall mortality of 80–90%. Rupture into the peritoneal cavity is usually rapidly fatal, whereas retroperitoneal rupture may transiently stabilise, providing a window of opportunity for lifesaving intervention. Patients should be transported to a vascular surgical centre immediately, and hypotensive resuscitation instituted to prevent excessive blood loss. Nevertheless, the majority of patients die before arrival at a surgical centre.
Mortality with open repair for ruptured AAA has stabilised at 30–40%
Clinical Presentation and Examination
Shock
Management
Resuscitation
Urgent Surgical repair
Open repair
Side note Open repair involves replacement of the diseased aortic segment with a tube or bifurcated prosthetic graft, through a midline abdominal or retroperitoneal incision
Prevention of AAA
Risk Factors for AAA
Advancing age
Male gender
Smoking
Family history
Atherosclerosis
Hypertension
Hypercholesterolaemia
Other vascular aneurysm
What is an aortic dissection?
occurs when a tear in the tunica intima of the aorta causes blood to flow between the layers of the wall of the aorta, forcing the layers apart.
What is a false lumen, and how does this occur
The area where blood collects between the tunica intima and media
High-pressure blood shears more of the tunica intima of the tunica media, blood starts to pool between the two layers increasing the outside diameter of the blood vessel.
Causes of Aortic Dissection
Chronic Hypertension: due to stress, increased bp, coordination
Weakened aortic wall: Marfarn’s syndrome, Ehlers-Danlos syndrome, Decreased blood flow in vasa vasorum
Aneurysms
Where do aortic dissection most often occur
First 10cm of aorta closest to heart
Classifications of aortic dissection
Type A: First 10cm of aorta, closest to heart
Tybe B: tears in descending aorta
Complications of Aortic Dissection
Cardiac tamponade
Aortic incompetence
MI
Aneurysmal degeneration/rupture
Regional ischaemia
Endoleak
Symptoms of Aortic dissection
Sharp chest pain-radiate to back
Weak pulse in a downstream artery
Diff in BP between left & right arm
Hypertension
Shock (If there is a rupture)
Investigations to identify aortic dissection
Widened aorta on chest xray
Transoesophageal echocardiogram
CT angiography
Magnetic resonance angiography Gold Standard
Pathophysiology o aortic dissection
Treatment for aortic dissection
A: Surgery
B: Beta-blockers, Nitroprusside
EVAR= Endovascular Aortic Repair
Diagnosis of aortic dissection
Risk Factors of aortic dissection
High bp
Connective Tissue Disorder
Aneurysms
What is an arrhythmia
Loss of rhythym - abnormal heart rhythym
What is bradycardia
<60bpm
What is tachycardia
> 100bpm
Mechanism of bradyarrhythmia
- Reduced automaticity: Athletes, sleeping, diseases, medications
- Conduction Block: AV node, Bundle of His
Mechanism of tachyarrythmia
- Increased automaticity
- Triggered activity
- Reentry
How can you classify tachyarrhythmias
based on location
Supraventricular: originate from the atrium and AV node above the ventricles
Ventricular: originate below AV node on the ventricular level
How can you characterise tachyarrhythmias on an ECG
Supraventricular: Normal -appearing or narrow QRS complexes
Ventricular: Abnormal appearing, prolonged QRS complexes
Examples of supraventricular tachycardia
Atrial fibrillation
Atrial flutter
Atrial tachycardia
AVRT
Atrioventricular Nodal Entry tachycardia (AVNRT)
How is atrial fibrillation diagnosed (ECG findings)
Finding of an irregularly irregular ventricular rhythym without discrete P waves
Iso electric line is not straight and is characterised by F waves
Narrow QRS complex
What is atrial fibrillation? The result of
ectopic foci: will fire rapid impulses to the AV node cancelling normal impulses that are generated; thus, the AV node will pick up impulses irregularly, resulting in an unsynchronised rhythm and rapid ventricular rate
reentry circuit in the atrial myocardium: this could be due to ischaemic heart disease, age, hypertension changing atrial morphology. Results in slow conduction area having a slower refractory period. AV node will capture impulses in irregular intervals resulting in a rapid irregular rate.
Investigations AF
ECG - changes in AF or MI
ECG shows absent p waves, irregularly irregular rhythm, QRS (typically narrowed). Rate is usually about 150bpm
Echocardiogram - valvular heart disease
Chest x-ray - heart failure
Troponin - MI?
ABG - if shocked, hypoxic or signs of acidosis
For non-cardiac causes
Thyroid function test
Full blood count - ↑WCC (pneumonia)
EUC - hypokalaemia +/- renal impairment
Other investigations when the patient is stable
24-hour ambulatory monitor to assess heart-rate control and look for episodes of symptomatic bradycardia
Exercise test (or other ischaemia stress test)
Coronary angiography
Cardiac magnetic resonance.
What causes atrial flutter
ECG presentation of individual with atrial flutter
No normal P waves. F waves present
Narrow QRS complex
Complications with Atrial Flutter
Management of Atrial Flutter
Using the Bundle of Kent, the ventricles undergo…
Pre-excitation
Left Side: Type A pre-excitation. More common
Right Side: Tybe B pre-excitation
So on an ECG people with WPW have..
Short PR interval with a delta wave ,<120ms
QRS prolongation, >110ms
ST segment and T wave will be often be directed opposite the QRS complex
Causes of WPW Syndrome
Reentry circuit: Signal moves back up Bundle of Kent
The type of reentry circuit where electrical conduction goes from the ventricle to the atrium is called Atrioventricular reentrant tachycardia (AVRT) with orthodromic conduction. This leads to high ventricular rates
You can also get Atrioventricular reentrant tachycardia (AVRT) with Antiidrmoic conduction when
Treatment for WPW
Pharmacological
Definitive treatment is radiofrequency catheter ablation of the Bundle of Kent.
Complications of WPW
What are the diff types of AVNRT
Slow-fast AVNRT: most common (90%)
There is anterograde conduction by slow AV nodal pathway and retrograde conduction by the fast nature of AV pathway
Fast Slow AVNRT: There is antergrade conduction by the fast AV node. Retrograde conduction by slow AV node pathway
ECG findings on AVNRT
Absent P wave
Narrow QRS
High amplitude QRS
HR is 150bpm
Acute management for AVNRT
unstable patient: Cardioversion with amiodarone infusion
Management of AVNRT of a stable patient
- Vagal Manouevers
-Valsalva Manoeuvre - Intravenous adenosine
Examples of Ventricular tachycardia
Ectopic VT: single beats from ventricles
Focal VT: abnormal automaticity
Re-entrant VT: see pic
ECG findings for VT
Monomorphic VT~reentrant + focal (one point)
Polymorphic VT~ focal (multiple areas)
Treatment of VT
What is 1st degree AV block
Delay in conduction through the AV node
In an ECG- PR interval >200ms
ECG findings of Mobitz 1 AV block
Progressively longer PR interval (progressive fatigue of AV cells)
non-conducted ventricular beat
Cyclical, e.g. 4:3 P:QRS
ECG findings on Mobitz II AV block
PR interval is constant
Intermittent non conducted P wave
May have fixed ratio P:QRS
*Below Bundle of His in 75% -Wide QRS
Within Bundle of His in 25% - narrow QRS
ECG findings on Complete Heart Block
Junctional/ventricular escape rhythym
No correlation of P waves and QRS complexes
No. of P waves > QRS complexes
Summary of ECG findings on heart blocks
First Degree = Far away P.
Wenckebach = Longer then Drop.
Second Degree = Drop Randomly.
Third Degree = Beat Independently.
What happens in Right/Left Bundle Branch Block
Vice versa
Lead II (Limb lead) ECG findings on a bundle branch block
Precordial ECG findings of left bundle Branch Block
(WiLLiaM/MaRRoW)
V1: No R wave. W
V6: Notched QRS. M
Precordial ECG findings of right bundle Branch Block
(WiLLiaM/MaRRoW)
V1: Terminal R wave. M
V6: Slurred S wave. W
Signs and symptoms of hypertension
Hypertension is a common disorder that affects a large proportion of the community. It is usually asymptomatic and is detected on routine examination or after the occurrence of a complication such as a heart attack or stroke. It is often referred to as the silent killer.
Remember Several things can cause bias to the hypertension readings (White coat hypertension). In the clinic, usually the 1st measurement is disregarded and the average of the second and third readings are taken.
Risk Factors for hypertension
Obesity
High alcohol intake
Metabolic syndrome
Diabetes
Dyslipidaemia
High sodium intake
Sleep apnoea
Increasing age
Family history
The differential diagnosis for hypertension
Primary (essential) hypertension
Secondary Hypertension (underlying, often reversible cause)
Causes of secondary Hypertension
Secondary hypertension
In a minority of cases, an underlying, often reversible cause can be found.
Vascular
Renal Artery Stenosis
Coarctation of the aorta
Pre-eclampsia
Think Renal artery stenosis should be suspected if BP is unexpectedly low or kidney function deteriorates in patients taking an ACEI or ARB.
Kidneys
Chronic Kidney Disease
Nephrotic Syndrome
Nephritic Syndrome
Obstructive Uropathy
Polycystic Kidney Disease
Endocrine
Phaeochromocytoma
Hyperaldosteronism
Cushing’s Disease
Hyperthyroidism
Toxic causes
Chronic alcohol use
Long term NSAIDs
Oral contraceptive pill
Illicit medication such as cocaine or Amphetamines
Obstructive sleep Apnoea
Pseudo-hypertension
Pathology of hypertension
- Thickened internal elastic lamina
- Smooth muscle hypertrophy and fibrosis -> decreased wall compliance
- As hypertension progresses, vessels experience vascular changes, remodelling and hypertrophy.
- Plaque build-up and hypertrophy + narrowing of the lumen and build-up of vascular pressure resulting in hypertension
Investigations for hypertension
Think: Although in the majority of patients, hypertension is primary/essential, certain features may lead to a suspicion of an underlying cause (secondary hypertension):
Young patient (<40 years)
Rapid onset of hypertension
Sudden change in blood pressure readings when previously well controlled on a particular therapy
Resistant hypertension that is unresponsive to pharmacological therapies
Investigations
ECG – may show evidence of LVH or old infarction
GFR - monitor kidney function
Fasting lipid - High fat is associated with hypertension
Urinalysis – proteinuria may indicate end-organ damage
Hb – Anaemia may indicate CKD, polycythemia may indicate Phaeochromocytoma
Plasma renin – low renin suggests hyperaldosteronism
Plasma aldosterone (with hypokalaemia and high sodium) – suggests hyperaldosteronism
Renal duplex ultrasound – may show renal artery stenosis, renal scarring or lesions
Thyroid function test
Sleep study
24-hour urine-free cortisol
Management of hypertension
Management of chronic hypertension
Education
Sodium reduction
Diet – high fruit and veg, whole grains, low sodium, low-fat proteins
Waist circumference reduction
Increase physical activity – 30 min a day
Limit alcohol consumption
Smoking cessation
Management of sleep apnoea
Monitoring
The cornerstone of managing primary hypertension is modifying poor lifestyle choices (i.e. diet, smoking cessation).
Antihypertensive medications are recommended for patients with a high risk of cardiovascular disease and moderate-severe hypertension. Secondary causes of hypertension may require surgery and additional medications.
Follow up in 3 months, then every six months thereafter
Antihypertensives first-line Patients commonly require two or more combined drugs to reach BP targets.
Ace inhibitors/ARBs
Calcium Channel Blockers
Beta-blockers are added as secondary
Thiazide (typically for coexisting Congestive Heart Failure)
Initiate hypertensives immediately if hypertension grade III
Remember: Combining an ACEI or ARB, a diuretic, and a nonsteroidal anti-inflammatory drug – the triple whammy – can cause acute kidney failure.
What is a complication of deep vein thrombosis
Acute
Pulmonary Embolism
Phlegmasia cerulea dolens (acute limb gangrene)
Chronic
Post-thrombotic syndrome
Chronic venous insufficiency
Signs and symptoms of deep vein thrombosis include
Clinical Presentation DVT usually affects the veins in the legs, notably the calf.
Asymmetrical pain and/or tenderness
Asymmetrical warmth/ erythema
Asymmetrical swelling
-Signs of Pulmonary embolism (a complication of DVT)
Breathlessness
Chest pain
Coughing
Tachycardia
Haemoptysis
Aetiology of deep vein thrombosis
All comes down to Virchow’s Triad. Any change to Virchows triad increases the risk of VTE.
Virchows Triad: Hypercoagulability, Vessel wall injury, Stasis
–Hypercoagulability
Malignancy
Surgery
Trauma
Oral contraceptive pill
Genetic
Antiphospholipid syndrome
Hyper homocysteine level
Inherited Thrombophilia
Factor 5 leiden mutation
Prothrombin gene mutation
Protein S deficiency
Protein C deficiency
–Stasis
Immobility, e.g. after surgery
Pregnancy
Obesity
Heart failure
Cast on the leg
Extended travel in plane/vehicle
–Endothelial injury
Inflammation
Previous thrombosis
Atherosclerosis
Fracture
Risk Factors of deep vein thrombosis
genetics:
-prothrombin gene mutation
- protein c or s deficiency
- Antithrombin deficiency
Investigations for deep vein thrombosis
Serology tests: FBC, LFTs, EUC, INR, APTT
Venous duplex ultrasound
Contrast venography gold standard
D-DIMER assay - rule out pulmonary embolism
Think D-dimer assay is only useful if it is negative; it helps rule out DVT.
Management of deep vein thrombosis
The aim of treatment is to prevent PE, reduce morbidity and prevent or minimise the risk of developing the postphlebitic syndrome
Pain management - analgesia +/- opioids
Anticoagulation
Low risk bleeding - Low molecular weight heparin (enoxaparin 1.5mg/kg SC daily)
Average risk bleeding - Unfractionated heparin
Signs and symptoms of pulmonary embolism
Clinical Presentation
Most patients with PE experience dyspnea commonly without other symptoms. Syncope, cyanosis, and angina are signs of massive PE. Unilateral pleuritic chest pain is experienced in the minority of patients +/- haemoptysis. Signs and risk factors for DVT are vital during history and examination.
Remember: Always suspect pulmonary embolism (PE) in sudden collapse 1-2 weeks after surgery.
Examination
Hypotension, ↑JVP indicates massive PE with pulmonary hypertension
Tachycardia
Dyspnea (breathlessness)
Pyrexia following lung infarction is common
Signs of DVT - pain, swelling, and erythema to the lower extremity, particularly the back of the leg below the knee
How would a pulmonary embolism appear on an xray
Dilated pulmonary vessels
Pleural effusion
Dilated hemi-diaphragm
Wedged opacity
Risk Factors of developing pulmonary embolism
Pulmonary Embolism usually arise from Deep Vein Thrombosis (DVT). DVT is the most common in patient over 40 years of age who undergo major surgery
Pregnancy
Increasing Age
Immobility
Cardiopulmonary Disease
Malignant disease
Surgery
Fractures
Varicose veins
Remember Genetic predisposition to hypercoagulability accounts for approximately 20% of PEs. The most common inherited conditions are the factor V Leiden mutation and the prothrombin gene mutations
Investigations for PE
CT Pulmonary Angiogram (Gold Standard)
V/Q Perfusion Scanning
D-Dimer Assay - Helps ruling out PE
Chest X-ray - May look normal
ECG
Investigations Radiologic studies are critical in the diagnosis of PE and DVT. A normal or near-normal chest x-ray is the most common finding in PE. Classic abnormalities associated with PE include Westermark sign (nonspecific prominence of the central pulmonary artery with decreased pulmonary vascularity), Hampton hump (peripheral wedge-shaped density above the diaphragm), and Palla sign (enlargement of the right descending pulmonary artery). D-dimer is not specific for DVT, but can help in ruling PE out.
Management of pulmonary embolism
General management:
100% oxygen sitting up (patients may need intubation)
Fluids
Opiates
Anticoagulants
Unfractioned heparin IV continous infusion (check APTT regularly 4-6 hours) OR
Subcutaneous low-molecular-weight heparin - rapid onset (no monitoring generally required)
Warfarin (Oral) after patient is stable (check INR)
Look for cause of PE
Remember Normal INR is 1. Therapeutic range for people on warfarin INR 2-3
Emergency Pulmonary Embolism If patient is haemodynamically unstable, emergency pulmonary embolectomy should be considered. In patients with large PE and no contraindications, thrombolysis is the definitive management.
In patients who are do not require or are contraindicated for emergency pulmonary embolectomy or thrombolysis therapy the general management approach include high flow oxygen and IV heparin. Oral warfarin is started once patient is stable. Heparin works by inhibiting the several steps of the common clotting pathway. Warfarin is a vitamin K reductase antagonist and therefore inhibits the synthesis of several clotting factors in the liver. Vitamin K reductase is an enzyme that activates vitamin K. Vitamin K is important in the production of several clotting factors (II, VII, XI, X)
Diagnosis for Peripheral Vascular Disease
CT angiography = Gold standard
Management for Peripheral Vascular Disease
What does acute Pericarditis result in
Friction Rub
Changes in ECG: ST elevation & PR depression followed by T wave flattening and inversion
Risk Factors for pericarditis
Remember Patients with systemic autoimmune disease can have multiorgan involvement, such as pericarditis, nephritis, pleuritis, arthritis, and skin disorders.
Signs and symptoms of pericarditis
Fever and malaise
Sharp retrosternal or left-sided chest pain.
The pain is often eased by leaning forward and is worse in the supine position
“pericardial rub” -friction rub on auscultation, often transient -
Tachycardia
Remember Acute Pericarditis triad: chest pain, friction rub and ECG changes
Pericarditis causing pericardial effusion can show
Signs of right sided heart failure - ↑JVP, peripheral oedema
Paradoxical pulse (systolic blood pressure decreases by more than 10 mm Hg during inspiration)
Causes of Pericarditis
(CARDIAC RIND)
Complications of pericarditis
Pericardial effusion
Cardiac Tamponade
Chronic constrictive pericarditis
Symptoms similar to pericarditis
Investigations for Pericarditis
Remember Prompt echocardiography may be required to determine the presence and amount of pericardial fluid.
FBC
EUC
LFT
X-ray
Echocardiogram
Troponin and other cardiac markers
Management of pericarditis
NSAIDs + PPIs help relieve symptoms
Colchicine and steroids are also used for as adjuncts and for more serious cases
For resistant recurrent pericarditis, seek specialist advice.
In symptomatic pericardial effusion and cardiac tamponade cardiocentesis is performed.
Signs and Symptoms of pericardial effusion
Key presentations:
Obscured apex beat
Heart sounds are soft
Pleuritic pain - exacerbated when lying down, better when sitting up
Diagnosis of pericardial effusion
Treatment for pericardial effusion
Prevention of infective endocarditis
antibiotic prophylaxis with amoxicillin orally or ampcillin IV/IM 1 hour before procedure
Acquired Heart Valve Disease
Aortic Valve Disease
Aortic Stenosis
Aortic Regurgitation (Incompetence)
Mitral Valve Disease
Mitral Stenosis
Mitral Regurgitation (incompetence)
Other Heart Valve Disease
Infective Endocarditis
Rheumatic Fever
Clinical Presentation of valvular disease
Clinical auscultation of valvular disease
Examination of a patient suspected with aortic stenosis
Slow Rate of rise in carotid artery
Reduced intentsity of 2nd heart sound on ausculatation of right 2nd intercostal space parastenal
*Right 2nd intercostal space murmur
*systolic click crescendo decrescendo murmur (ejection systolic murmur)
Aetiology of aortic stenosis
1.Congenital abnormal valve (unicuspid/bicuspid)
- Calcification of tricuspid valve
- Rheumatic valvular disease
Investigations for aortic stenosis
ECG: may show left ventricular hypertrophy
Cardiac catheterisation
Transthoracic echocardiogram GOLD STANDARD
Management for aortic stenosis
Surgical Valve replacement: mechanical, bioprosthetic
Long-term anticoagulants
Inoperable patients:
Balloon valvuloplasty
Trans catheter valve replacement
What is aortic regurgitation
Characterised by the backflow of blood into the right atrium during systole
Causes of primary aortic regurgitation
+ Marfan Syndrome
Causes of secondary/functional aortic regurgitation
*Pulmonary Hypertension
*Dilation of the tricuspid annulus
Pathophisiology of aortic regurgitation
Clinical examination of aortic regurgitation
Investigations for aortic regurgitation
Treatment for aortic regurgitation
Aside from open heart surgery trans-catheter options: annuloplasty, valve replacement, coaptation device
Aetiology of mitral regurgitation
Signs and symtpoms of mitral regurgitation
Examination findings of mitral regurgitation
*Diminished S1 Heart Sounds
Flat continuous murmur in systole (pain/holosystolic murmur). Murmur radiates to left axilla
Management of mitral regurgitation
Preoperative diuretic
Valvuloplasty
Valve Repair/Replacement
Annuloplasty
Intra-aortic balloon counterpulsation
Signs of shock
Physiologic change of shock
Treatment for shock
Pneumonic: ABCDE
Airway: ensure clear airway, possibly intubate
Breathing: assist an individual in breathing, mechanical ventilation/sedation
Circulation: administer fluids
Delivery of oxygen: monitor lactate levels
Endpoint resuscitation (specific to septic shock)
What are the determinants of myocardial performance
Preload: Amount of blood entering ventricles during diastole -> End Diastolic Volume
Afterload: Force ventricles must overcome
Contractility
What causes hypertrophic cardiomyopathy
Autosomal mutation of genes coding for sarcomere proteins
Secondary causes: chronic hypertension ->
Increase in afterload -> Hypertrophy of left ventricle
Freidrich’s ataxia: Autosomal recessive neuro generative mutation of frataxin gene
Fabry’s disease
Mechanism of disease for hypertrophic cardiomyopathy
Clinical manifestation of hypertrophic cardiomyopathy
More pronounced symptoms when exercising: syncope, angina, dyspnea
Investigations for hypertrophic cardiomyopathy
ECG
Echocardiagram
Cardiac MRI
Treatment for hypertrophic cardiomyopathy
Clinical manifestations of dilated cardiomyopathy
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
S3 Gallop
What do you see on an echocardiogram with a patient having dilated cardiomyopathy
Signs and symptoms of restrictive cardiomyopathy
Cardiomyopathy table
Signs and symptoms of rheumatic fever
Diagnosis of Rheumatic fever
Treatment for rheumatic fever
What is tetralogy of Fallot
Symptoms of Tetralogy of Fallot
Baby:
Cyanosis to lips + fingertips
Clubbing in fingers & toes
Any decrease in O2
Cyanotic Spell: relieved with squatting down
Causes involving adult coarctation
Upstream:
-Risk of Berry aneurysm
-Risk of aortic dissection
Downstream
Hypertension
Diagnosis of coarctation of aorta
Treatment of coarctation of aorta
Signs and symptoms of Patent ductus arteriosus
Diagnosis of Patent Ductus Ateriosus
Treatment of Patent Ductus Arteriosus
Pathology and Causes of Ventricular Septal Defect
Defects in the ventricular septum that allows shunting of blood between the RV and LV.
Causes:
Congenital
Rarely acquired after MI or trauma
Signs and symptoms of Ventricular Septal Defect (VSD)
Diagnosis of Ventricular Septal Defect
Echocardiogram = Gold Standard
Treatment of Ventricular Septal defect
Medically initially, since many will spontaneously close
Surgical closure
If small, no intervention is required
Prophylactic antibiotics
If moderate lesion, the following is sufficient: Furosemide, ACE-I e.g. Ramipril, Digoxin
Pathology and Causes of Atrial Septal Defect
Signs and Symptoms of atrial septal defect
Diagnosis of atrial Septal Defect
Treatment of atrial Septal Defect
Pathology and causes of Long QT syndrome
When ventricular repolarisation is greatly prolonged
Congenital
- Jervell-Nielsen syndrome (mutation if cardiac potassium & Na+ channel genes)
- Romano-Ward syndrome
Acquired
- Hypokalaemia
- Hypocalcaemia
- Drugs e.g. tricyclic antidepressants
- Bradycardia
- Acute MI
- Diabetes
Risk Factors of Long QT interval
Diagnosis of Long QT interval
Serum electrolytes : Hypokalaemia, hypomagnesaemia, hypocalcaemia may be present
Pathology and Causes of Torsades des pointes
“Twisting of points”. Associated w/ long QT syndrome
Causes
Congenital (LQT1, LQT2 etc)
Certain medications (Class 1a anti-arrhythmic drugs)
Risk Factors of Torsades des Pointes
ECG findings on Torsades des Pointes
Chest X ray findings for heart failure
