Cardiology Flashcards
(420 cards)
1
Q
What is atherosclerosis
A
Hardening/narrowing of arteries due to plaque
2
Q
Clinical Presentation of atherosclerosis
A
3
Q
Risk factors of atherosclerosis (7)
A
Age
Tobacco smoking
High serum cholesterol
Obesity
Diabetes
Hypertension
Family history
4
Q
Complications of Atherosclerosis
A
Gangrene
Stroke
Heart attack
5
Q
Structure of an atherosclerotic plaque
A
Lipid
Necrotic core
Connective tissue
Fibrous cap
6
Q
What causes LDL being deposited in atherosclerosis
A
Endothelial dysfunction
7
Q
Summarise the main stages involved in the formation of an atherosclerotic plaque
A
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.
8
Q
Describe the progression of atherosclerosis
A
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
9
Q
What is a limiting factor to treating coronary artery disease?
A
Restenosis: Drug-eluting stents improve the duration of stents; anti-proliferative and inhibit healing
10
Q
Useful drugs in treating coronary artery disease
A
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.
11
Q
Major cell types involved in atherogenesis are …
A
endothelium, macrophages, smooth muscle cells and platelets
12
Q
Name the nodal cells
A
SA node
AV node
AV bundle (Bundle of His)
Bundle branches (L&R)
Purkinje fibers
13
Q
State the pacemakers of the heart
A
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
14
Q
Who sets the sinus rhythm and how many bpm
A
SA node. 60-100bpm
15
Q
Action potential from SA node goes to…. and what happens as a result
A
Bachman’s bundle: Depolarises the LA
Internodal branches: Depolarise RA
16
Q
The SA bundle sends action potential to the rest of Right atrium via the
A
Internodal pathway
17
Q
What does Limb lead 1 show activity of?
A
High lateral wall of LV
18
Q
Where does the internodal branch converge?
A
AV node
19
Q
What is the importance of AV node
A
Acts as a gateway between atria and interventricular septum
20
Q
What is the importance of AV node delay
A
Want to give time for the atria to contract before the ventricles contract
21
Q
How is AV node delay created?
A
Has fewer gap junctions than other nodal cells
Have a smaller diameter (slower conduction speed)
22
Q
What does Limb lead 2+3 show activity of
A
Inferior wall of the heart
23
Q
Cardiac conduction system
A
- SA node
- AV node
- Bundle of His
- L/R Bundle branches
- Purkinje fibers
24
Q
What does aVR show activity of?
A
RV + Basal septum
25
What does aVL show activity of?
High lateral wall of LV
26
What does aVF show activity of?
Inferior wall of the heart
27
Where would you place V1
right 4th intercostal space, parasternal space
28
Where would you place V2
Left 4th intercostal space (parasternal line)
29
Where would you place V3
Between V2 + V4
30
Where would you place V4
left 5th intercostal space, mid clavicular line
31
Where would you place V5
Left 5th intercostal space, anterior axillary line
32
Where would you place V6
Left 5th intercostal space, mid axillary line
33
What is happening to the R wave as you go through V1-V6
Getting bigger
34
What is happening to the S wave as you go through V1-V6
Getting smaller
35
What do V1-V3 tell us about the activity?
RV
36
What limb leads tell us about the right ventricle
V1-V3
aVR
37
What does V2-V3 tell us about the activity of?
Basal septum
38
What limb leads tell us about the basal septum
V2-V3
aVR
39
What limb leads tell us about the anterior wall of the heart
V2-V4
40
What does V2-V4 tell us about the activity of?
Anterior wall of heart
41
What does V5-V6 tell us about the activity of?
LV
42
What limb leads tell us about the LV
V5-V6
Limb lead 1
aVL
43
How long should PR interval be?
<=0.2 secs
44
How long should QRS wave be?
<=0.12 secs
45
What is the Electrocardiogram?
a measure of the currents generated in the EXTRACELLULAR FLUID by the changes co-occurring in many cardiac cells
46
What is a P Wave?
Atrial depolarisation - seen in every lead apart from aVR
47
What is the PR Interval?
Time taken for atria to depolarise and electrical activation to get through AV node
48
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
49
What is the ST Segment?
Interval between depolarisation & repolarisation
50
What is the T wave?
Ventricular repolarisation
51
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
52
What happens to the ST segment in an Acute Inferior Myocardial infarction?
ST segments are raised in inferior (II, III, aVF) leads
53
Why is atrial repolarisation usually not evident on an ECG?
since it occurs at the same time as the QRS complex so is hidden
54
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)
55
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
56
Are P waves positive?
In a normal ECG the p waves are POSITIVE in EVERY LEAD (apart from the aVR)
57
What is angina?
Chest pain thats felt due to lack of blood flow to the heart muscle
58
What causes angina?
Reduced blood flow, which causes ischaemia in the heart muscle
59
Different types of angina?
Stable
Unstable
Prinzmetal's angina
60
Which is the most common type of angina
Stable angina
61
When does stable angina occur?
When the patient has greater than or equal to 70% stenosis (blocked by plaque build up)
62
When do individuals with stable angina experience chest pain?
During exercise or stress as the heart works harder
The pain goes away with rest
63
What is the underlying cause of stable angina?
atherosclerosis of one or more coronary artery
64
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
65
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
66
Where is pain felt in a patient with stable angina
Pressure or squeezing
left arm, jaw, shoulders, back
67
Alongside pain what else can a patient with stable angina experience
Shortness of breath
Diaphoresis
68
How long does stable angina last?
20 mins
subsides after exertion or stress taken away
69
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
70
How is unstable angina caused ?
Rupture of atherosclerotic plaque with thrombosis
71
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
72
What is the key differentiation of angina from myocardial infarction?
Angina: heart tissue is alive but ischaemic
Myocardial infarction: tissue has begun to necrose
73
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
74
When does a patient with vasospastic angina feel pain
Anytime
75
What is a classic presentation of patients with vasospastic (Prinzmetals) angina
Transmural ischaemia: Entire thickness of myocardium
76
Table explaining simarilities/differences of angina
Also in stable and unstable angina the no of cardiac markers (troponin) are not elevated
77
Risk Factors for angina
78
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
79
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
80
Complications for angina
Acute Coronary Syndrome
81
What is Acute Coronary Syndrome
Reduction/loss or total occlusion of blood supply to the heart muscle
82
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)
83
Is Acute Coronary syndrome considered a medical emergency ?
Yes
84
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.
85
What are the risk factors of developing acute coronary syndrome
86
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
87
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
88
Causes of chest pain by body systems
89
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
90
Why is measuring troponin levels important?
useful and important in diagnosing STEMI and NSTEMI
91
What do we refer to as acute coronary syndrome
STEMI
Non STEMI
Unstable angina
92
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.
93
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
94
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.
95
Where does myocardial infarction tend to occur?
1.LAD
2.RCA
3.LCX
96
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**
97
Describe an NSTEMI regarding ischaemia and infarction
Infarction distally
Ischaemia proximally
To artery supply
Leads to subendocardial infarction
98
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**
99
Describe a STEMI regarding ischaemia and infarction
Infarction distally & Infarction proximaly to the artery supply
Leads to transmural infarction
100
What does New LBBB regarding STEMI suggest?
Infarction of the septum of the heart where the left bundle branch goes through
101
Pathophysiology of acute coronary syndrome
102
Describe the presence of cardiac markers in:
Unstable angina
NSTEMI
STEMI
Unstable Angina: No increase
NSTEMI & STEMI: Increase
103
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)
104
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
105
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).
106
What is heart failure?
Used to describe an point at which the heart cant supply enough blood to meet the bodys demands
107
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
108
What is systolic heart failure?
When the heart cannot pump hard enough
The ejection fraction is below 40% due to Stroke Volume decreasing
109
What is ejection fraction?
Stroke Volume/Total Vol
Normal: 50%-70%
Borderline: 40%-50%
Systemic Heart Failure: >40%
110
What is Diastolic Heart Failure?
The heart cannot fill with enough blood
Low Stroke Volume but Normal Ejection Fraction. Due to reduced preload
111
What is an important relationship between systolic and diastolic function?
Frank Starling mechanism
112
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
113
Pathophysiology of heart failre
114
Classification of heart Failure
115
What are heart failure cells called
Haemosiderin-Laden macrophages
116
Left vs Right heart Failure
CVP = Central Venous Pressure
PAP= Pulmonary Arteriole Pressure
117
Diastolic vs Systolic heart failre
118
Diagnosis of heart Failure
Primarily a clinical diagnosis
1. History
2. Physical exam:
bilateral lung crackles
peripheral pitting oedema
rasised JVP
Additional heart sounds: S3 dilation, S4 poor LV compliance
3. Lab markers
NtproBNP
-Prognostic: 22.5% mortality if >5000pg/ml
4. Imaging: Chest x ray, echocardiogram
119
Treatment of heart failure
Preload: diuretics
Afterload: ARBs/ACEi & BB
Neurohorm
Inotrope: norepinephrine/dopamine
Contractility
Device
Rhythm
Anticoagulation/antiplatelet
Iron Studies
Risk reduction
120
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
121
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
122
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
123
Clinical Manifestations of cor pulmonale
124
Investigations for cor pulmonale
125
Differential diagnosis for cor pulmonale
COPD
Pneumonia
Pulmonary embolism
126
Left-sided Heart Failure, blood gets backed up into ____
Right-sided Heart Failure, blood gets backed up into ____
Lungs
Body
127
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.
128
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
129
Complications for cor pulmonale
RV failure
Liver dysfunction
130
Treatment for Right Sided Heart Failure
ACEi
Diuretics
131
Heart Failure causes a...
arrhythmia: Ventricles out of sync
132
Signs and symptoms of heart failure (6)
133
Treatment for Diastolic Heart Failure
Cardiac resynchronisation therapy with patients suffering from arrhythmia
Ventricular Assist Device
End Stage Heart Failure -> Heart Transplant
134
Treatment for Systolic Heart Failure
Cardiac resynchronisation therapy with patients suffering from arrhythmia
Ventricular Assist Device
End Stage Heart Failure -> Heart Transplant
135
Are the majority of people with Abdominal Aortic aneurysm symptomatic or asymptomatic?
Asymptomatic
It is often an incidental finding -> Needs monitoring
136
Where do Abdominal Aortic aneurysm start
90% Below renal artery
15% Extend to common iliac artery
137
What is an aneurysm
an artery that has enlarged to greater than 1.5 times the expected diameter
138
What is an abdominal aortic aneurysm (Triple A)
Defined as an aneurysm greater than 5.5cm
**Requires treatment**
139
What can an AAA progress to?
ruptured AAA
Anteriorly rupture into peritoneal cavity -> Fatal
Posteriorly rupture into retroperitoneal -> transiently stable
140
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
141
What is the prognosis of anterior AAA rupture
Poorer prognosis than posteriorly
142
Differential diagnosis of AAA
Acute Pancreatitis
Mesenteric Ischaemia
Ruptured gastrointestinal ulcer
Appendicitis
Gallstone Disease
Nephrolithiasis
Irritable Bowel Syndrome
143
Complications of AAA
AAA rupture
Death
Renal Failure
Lower limb ischaemia
Mesenteric ischaemia
144
Investigations for AAA
Abdominal ultrasound (definitive test)
ESR/CRP
FBC
CT
MRI
145
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
146
Prevention of AAA
147
Risk Factors for AAA
Advancing age
Male gender
Smoking
Family history
Atherosclerosis
Hypertension
Hypercholesterolaemia
Other vascular aneurysm
148
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.
149
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.
150
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
151
Where do aortic dissection most often occur
First 10cm of aorta closest to heart
152
Classifications of aortic dissection
Type A: First 10cm of aorta, closest to heart
Tybe B: tears in descending aorta
153
Complications of Aortic Dissection
Cardiac tamponade
Aortic incompetence
MI
Aneurysmal degeneration/rupture
Regional ischaemia
Endoleak
154
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)
155
Investigations to identify aortic dissection
Widened aorta on chest xray
Transoesophageal echocardiogram
CT angiography
Magnetic resonance angiography *Gold Standard*
156
Pathophysiology o aortic dissection
157
Treatment for aortic dissection
A: Surgery
B: Beta-blockers, Nitroprusside
EVAR= Endovascular Aortic Repair
158
Diagnosis of aortic dissection
159
Risk Factors of aortic dissection
High bp
Connective Tissue Disorder
Aneurysms
160
What is an arrhythmia
Loss of rhythym - abnormal heart rhythym
161
What is bradycardia
<60bpm
162
What is tachycardia
>100bpm
163
Mechanism of bradyarrhythmia
1. Reduced automaticity: Athletes, sleeping, diseases, medications
2. Conduction Block: AV node, Bundle of His
164
Mechanism of tachyarrythmia
1. Increased automaticity
2. Triggered activity
3. Reentry
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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
166
How can you characterise tachyarrhythmias on an ECG
Supraventricular: Normal -appearing or narrow QRS complexes
Ventricular: Abnormal appearing, prolonged QRS complexes
167
Examples of supraventricular tachycardia
Atrial fibrillation
Atrial flutter
Atrial tachycardia
AVRT
Atrioventricular Nodal Entry tachycardia (AVNRT)
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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
169
What type of arrhythymia is atrial fibrillation
Supraventricular tachyarrhythmia
170
What is atrial fibrillation?
Atria don't contract in a synchronous rhythm instead they "fibrillate"
-results in rapid, irregular heartbeat
171
Differential Diagnosis AF
Palpitations
Chronic atrial fibrillation
Paroxysmal atrial tachycardia
Atrial flutter
Wolff-Parkinson-White syndrome
Wolff-Parkinson-White syndrome has an extra electrical pathway in the heart (accessory pathway). The condition can lead to periods of tachycardia.
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Complication of atrial fibrillation
Clot formation and embolism due to stasis in the atrium
Left atrium is commonly involved in clot formation resulting in embolisation to brain causing stroke
173
Risk Factors for Atrial Fibrillation
Cardiovascular diseases:
High bp
Coronary heart disease
Valvular disease
Non-cardiovascular
Obesity
Diabetes
Excessive alcohol consumption
Genetic factors
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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.
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Classification of AF
Three clinical patterns (3Ps) All patterns have a risk of thromboembolism.
Paroxysmal AF: Defined as recurrent and terminates spontaneously within 24 hours -48 without any intervention
Persistent AF: Defined as AF that is sustained >7 days or lasts <7 days but necessitates pharmacological or electrical cardioversion
Permanent (Chronic) AF: refractory to cardioversion or accepted as a final rhythm. A decision has been made not to pursue restoration of sinus rhythm, including catheter or surgical ablation.
Remember, Chronic AF is having atrial fibrillation more than once. It may be paroxysmal, persistent, long-standing persistent, or permanent.
176
Risk Factors of AF (HIPSO)
Ischaemic Heart disease
Heart Failure
Pulmonary hypertension
Sleep apnea
Obstructive pulmonary disease
177
What is heart rate of individual with atrial fibrillation
100-180 bpm
178
What is the term used to describe a patient with AF and a fast heart rate
AF with rapid ventricular rate
179
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.
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What is the diagnosis for paroxysmal atrial fibrillation
Halter monitor
Implanted Loop recorder
181
What is the diagnosis for persistent atrial fibrillation
ECG
182
What is performed before a cardioversion and why?
Anticoagulation for 4 weeks or transoesophageal echocardiogram because a patient with AF >48 hours could have a thrombus formed.
If cardioversion takes place then thrombus can lodge causing stroke or mesenteric ischaemia
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(Pirates) Aetiology of AF
Pulmonary embolism, Pulmonary disease, Post-operative
Ischemic heart disease, Idiopathic (“lone atrial fibrillation”), IV central line (irritating the right atrium)
Rheumatic valvular disease (mitral stenosis or regurgitation)
Anemia, alcohol (“holiday heart”), Age, Autonomic tone (vagal atrial fibrillation)
Thyroid disease (hyperthyroidism)
Elevated blood pressure (hypertension), Electrocution
Sleep apnea, Sepsis, Surgery
184
Clinical presentation of atrial fibrillation
Clinical Presentation
Atrial fibrillation may cause chest pain, palpitations, dyspnea, or faintness. Signs include irregularly irregular pulse and possible signs of left ventricular heart failure. 30% of patients present with AF as an incidental finding only
Think AF may be associated with non-cardiac disease (i.e. pneumonia and hyperthyroidism)
Examination
Irregular pulse (which, if rapid, will be faster at the apex than the wrist)
The variable intensity of the first heart sound
Absent ‘a’ waves in the JVP
185
Outcome of acute management of AF
1. Person has reverted to normal sinus rhythym
2. Person still has AF
186
Complications of AF
Complications
Death
Bradycardia
Stroke
Heart failure
Hypotension
Amiodarone toxicity
Pulmonary Inflammation +/- Fibrosis
Thyroid Dysfunction
Remember 6Ps of Amiodarone side effects (6Ps): Prolongs action potential duration, Photosensitivity, Pulmonary fibrosis and inflammation, Pigmentation of skin, Peripheral neuropathy, Peripheral conversion of T4 to T3 is inhibited (Hypothyroidism).
187
What is atrial flutter
Atria contracts at high rates ~300bpm
188
What are the diff types of atrial flutters?
Type 1: typical atrial flutter
-Caused by a single reentrant circuit that moves around the tricuspid valve of the right atrium
-Counterclockwise
Type 2: Atypical atrial flutter
-Right or left atrium
-Exact location less defined
189
What causes atrial flutter
190
ECG presentation of individual with atrial flutter
No normal P waves. F waves present
Narrow QRS complex
191
Symptoms of Atrial Flutter
Shortness of breath
Chest pain
Dizziness
Nausea
192
Complications with Atrial Flutter
193
Management of Atrial Flutter
194
What is Wolff-Parkinson White Syndrome (WPW)
Type of heart arrhythmia caused by an accessory pathway called the Bundle of Kent allowing communication between the atria and ventricles
195
Using the Bundle of Kent, the ventricles undergo...
Pre-excitation
Left Side: Type A pre-excitation. More common
Right Side: Tybe B pre-excitation
196
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
197
Symptoms of WPW Pattern?
No symptoms
Usually benign
198
What does WPW Pattern sometimes facilitate
Certain arrhythmias
199
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
200
Incidence of WPW
~0.1%
201
Treatment for WPW
Pharmacological
Definitive treatment is radiofrequency catheter ablation of the Bundle of Kent.
202
Complications of WPW
203
What is AVNRT the result of
Abnormal unsynchronised electrical transmission from the AV node to the ventricles
Caused by a re-entry circuit in the AV node
204
What can trigger AVNRT
Differences in the slow and fast conduction pathway
205
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
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ECG findings on AVNRT
Absent P wave
Narrow QRS
High amplitude QRS
HR is 150bpm
207
Clinical Presentation of AVNRT
Palpitations
Diaphoretic
Haemodynamically unstable
Diuresis
208
Acute management for AVNRT
unstable patient: Cardioversion with amiodarone infusion
209
Management of AVNRT of a stable patient
1. Vagal Manouevers
-Valsalva Manoeuvre
2. Intravenous adenosine
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Management for recurrent AVNRT
Catheter ablation
211
What is ventricular tachycardia
type of arrhythmia orginating from the ventricles
-More than 3 consecutive premature ventriclar contractions
->100bpm
212
Examples of Ventricular tachycardia
Ectopic VT: single beats from ventricles
Focal VT: abnormal automaticity
Re-entrant VT: see pic
213
Complications of ventricular tachycardia
Less Filling -> Less pumped out each beat -> Less to Body & Brain
Results in: chest pain, fainting, dizziness, shortness of breath, sudden death
214
How are VT diagnosed?
ECG
215
ECG findings for VT
Monomorphic VT~reentrant + focal (one point)
Polymorphic VT~ focal (multiple areas)
216
What can VT lead to?
Ventricular fibrillation
217
Treatment of VT
218
What is Heart block
When conduction system through the electrical system of the heart is impaired
219
What is 1st degree AV block
Delay in conduction through the AV node
In an ECG- PR interval >200ms
220
Causes of 1st degree AV block
1. Increased vagal tone
2. Fibrosis
3. Drugs
4. Normal variant
5. coronary artery disease
6. mitral valve surgery
7. electrocyte imbalances: hypokalaemia, hypomagnesemia
221
Significance of 1st-degree AV block
Usually asymptomatic
Occasinal progression
x3 risk of developing atrial fibrillation
if symptomatic, a pacemaker is considered
222
2nd degree AV block types
Mobitz 1(wenckebach)
Mobitz 2 (Hay)
223
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
224
Causes of Mobitz 1 AV block
1. Increased vagal tone
2. normal variant
3. MI
4. Drugs
5. Mitral Valve surgery
6. Hypokalaemia
225
Significance of Mobitz 1 AV block
Doesn't require treatment
May cause bradycardia + hypotension, in which case atropine is used. Reduce AV blockers, pacing
226
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
227
Causes of Mobitz II AV block
Usually structural heart disease e.g fibrosis, myocardial ischaemia
228
Significance of Mobitz II AV block
Often symptomatic: syncope, fatigue, chest pain, death
High risk of progression
35% per year risk of asystole
Requires temporary pacing -> pacemaker
Atropine can precipitate Complete Block.
229
What is 3rd degree AV block (Complete Heart Block)
No association between atria + ventricles
230
ECG findings on Complete Heart Block
Junctional/ventricular escape rhythym
No correlation of P waves and QRS complexes
No. of P waves > QRS complexes
231
Causes of Complete Heart Block
1.Inferior MI
2.AV blocking agents
3.Degeneration of conduction system
232
Significance of Complete Heart Block
Often symptomatic: syncope, fatigue, chest pain, death
Atropine rarely effective - dopamine/adrenaline
Transcutaneous/transvenous pacing -> pacemaker
233
Summary of ECG findings on heart blocks
First Degree = Far away P.
Wenckebach = Longer then Drop.
Second Degree = Drop Randomly.
Third Degree = Beat Independently.
234
What is a bundle branch block?
Heart arrhythmia is where one or both bundle branches are delayed or blocked entirely, causing the ventricles to beat abnormally
235
Causes of Bundle branch block
Fibrosis (acute/chronic)
1.Acute: ischaemia & heart attack, myocarditis
2.Chronic: hypertension, coronary artery disease, cardiomyopathies = remodelling
236
Types of bundle branch Block
Right Bundle branch Block
Left Bundle Branch block
237
What happens in Right/Left Bundle Branch Block
Vice versa
238
Lead II (Limb lead) ECG findings on a bundle branch block
239
Precordial ECG findings of left bundle Branch Block
(WiLLiaM/MaRRoW)
V1: No R wave. W
V6: Notched QRS. M
240
Precordial ECG findings of right bundle Branch Block
(WiLLiaM/MaRRoW)
V1: Terminal R wave. M
V6: Slurred S wave. W
241
Significance of Bundle Branch Block
Present since birth
-Usually no symptoms/treatment
Acquired through heart disease
if accompanied by heart failure -> cardiac resynchronaisation pacemaker
242
What is hypertension defined as
Blood pressure >140/90 mmHg
243
Main goal of hypertension treatment
Decrease risk of morbidity and of cardiovascular and renal morbidity
244
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.
245
What is blood pressure
Product of cardiac Output and Peripheral Vascular Resistance
246
Risk Factors for hypertension
Obesity
High alcohol intake
Metabolic syndrome
Diabetes
Dyslipidaemia
High sodium intake
Sleep apnoea
Increasing age
Family history
247
The differential diagnosis for hypertension
Primary (essential) hypertension
Secondary Hypertension (underlying, often reversible cause)
248
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
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Pathology of hypertension
1. Thickened internal elastic lamina
2. Smooth muscle hypertrophy and fibrosis -> decreased wall compliance
3. As hypertension progresses, vessels experience vascular changes, remodelling and hypertrophy.
4. Plaque build-up and hypertrophy + narrowing of the lumen and build-up of vascular pressure resulting in hypertension
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Complications of hypertension
End organ damage
Hypertensive retinopathy
End organ damage
Cardiovascular disease
Cardiac failure
Left Ventricular hypertrophy
Cerebrovascular disease
Transient ischaemic attack
Cerebrovascular Attack
Renal failure
Retinopathy (Fundoscopy)
Arteriolar narrowing
Arteriolar venous nipping (nicking)
Cotton wool spots
Haemorrhages
Papilloedema
251
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
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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.
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Side effects: CCB & Beta blockers
Side effect of Beta blockers and Calcium channel blockers is orthostatic hypotension which is defined as a decrease in systolic blood pressure of 20 mm Hg or a decrease in diastolic blood pressure of 10 mm Hg within three minutes of standing when compared with blood pressure from the sitting or supine position.
254
Pharmacology: ACEi
Ace inhibitors work by inhibiting the membrane-bound enzyme ACE which usually converts Angiotensin I to Angiotensin II. Angiotensin II is a strong sympathomimetic increasing heart rate and contractility and a potent vasoconstrictor. Side effects of ACE include dry cough, hyperkalaemia, angioedema and rash (+/- nausea, diarrhoea, etc.). Contraindications include chronic cough, allergy, pregnancy and renal failure. An alternative drug for ACE is ARBs which work just as effectively.
255
What is a deep vein thrombosis
Deep Vein Thrombosis (DVT): Formation of a blood clot in one of the deep veins of the body, usually in the leg
256
Who are most at risk from developing deep vein thrombosis
Patients post op
Undergoing surgery
Bed bound patients
Patients with an immobile chronic illness
257
What is a complication of deep vein thrombosis
Acute
Pulmonary Embolism
Phlegmasia cerulea dolens (acute limb gangrene)
Chronic
Post-thrombotic syndrome
Chronic venous insufficiency
258
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
259
A leg with deep vein thrombosis will have
Oedema
Erythema
Warmth
260
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
261
What is the fate of a deep vein thrombosis (PORER)
Propagation: grow along vessel
Organisation: organising within the vessel layer
Recanalisation: forming holes within thrombus
Embolism: Dislodgement of the thrombus; travels around body via blood
Resolution: thrombus broken down by plasmin
262
How does deep vein thrombosis lead to a pulmonary embolism
Thrombus dislodges becoming an embolus.
Travels up heart via inferior vena cava
Heart will pump the embolus to pulmonary circulation
Embolus can lodge into pulmonary arteries causing pulmonary embolism
Can lead to pulmonary infarct
263
Risk Factors of deep vein thrombosis
genetics:
-prothrombin gene mutation
- protein c or s deficiency
- Antithrombin deficiency
264
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.
265
Differential diagnosis of a DVT
Cellulitis
Thrombophlebitis
Arthritis
Asymmetric peripheral oedema secondary to heart failure, renal disease or liver disease
Haematoma
Lymphoedema
Ruptured backers cyst
Varicose veins
266
Diagnosis of a DVT
Duplex ultrasound
Venography (phlebography) - Gold standard
267
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
268
Prevention of DVT
Identify patient at risk
Prevent Dehydration
Mechanical prophylaxis
Intermittent Pneumotic Compression
Calf compression stockings
Encourage movement
Exercise
Quit smoking
Medication - Warfarin to therapeutic dose INR 2-3 OR NOAC of choice
IVC filter
Prevention in surgery
High Risk - LMWH (40mg daily) + mechanical prophylaxis
Orthopaedic Surgery
Major trauma
Fracture
Major surgery >40yo
Medium Risk - LMWH (20mg daily) + mechanical prophylaxis
Low Risk - Consider LMWH + mechanical prophylaxis
All other surgery
Remember Make sure there are no contraindications for LMWH and Mechanical prophylaxis
269
What is a pulmonary embolism
Sudden occlusion in a pulmonary (Lung) artery
Occlusion is usually as a result of a blood clot that originated from DVT
270
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
271
How would a pulmonary embolism appear on an xray
Dilated pulmonary vessels
Pleural effusion
Dilated hemi-diaphragm
Wedged opacity
272
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
273
Differential diagnosis of PE
Acute Coronary Syndrome
Pneumothorax
Cardiac tamponade
Pneumonia
COPD
274
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.
275
Diagnosis of PE
PE is incorrectly diagnosed in almost 75% if patients. Acute onset of dyspnea or hypoxemia with a normal chest x-ray should be considered a pulmonary embolism until proven otherwise.
276
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)*
277
What is Peripheral Vascular Disease (PVD)
Condition used to describe when a blood vessel -besides those supplying heart or brain - become narrowed
278
Causes of Peripheral Vascular Disease
1. Atherosclerosis
2. Thrombo-embolism
3. Inflammatory conditions - Beurger's disease
279
Risk Factors of Peripheral Vascular Disease
Diabetes Mellitus
Hypertension
Hyperlipidaemia
metabolic syndrome
Smoking
Old Age
280
Clinical Presentations of Peripheral Vascular Disease
Intermittent claudication (most common)
Diminished or absent pulse when palpated
Dry, shiny skin with no hair
Thick, brittle nails
Dependent Rubor
Painful, regularly shaped, round ulcers
Elevation Pallor
281
What is referred to as the most severe stage of peripheral vascular disease
Critical limb ischaemia
282
Diagnosis for Peripheral Vascular Disease
CT angiography = Gold standard
283
Gold Standard Investigation for identfying peripheral vascular disease
Conventional Arteriography
284
Management for Peripheral Vascular Disease
285
Significance of Peripheral Vascular Disease
Asymptomatic until 70% Lumen obstruction
286
What is pericarditis?
Acute pericarditis: An inflammation of the pericardial sac surrounding the heart.
287
People who develop pericarditis are also at risk of also developing a
Pericardial effusion
288
What is pericardial effusion
Fluid that fills the pericardial space, which may be due to infection, haemorrhage, or malignancy. A rapidly accumulating effusion may lead to cardiac compromise.
289
What does acute Pericarditis result in
Friction Rub
Changes in ECG: ST elevation & PR depression followed by T wave flattening and inversion
290
What does constrictive pericarditis restrict
Heart relaxation
291
Risk Factors for pericarditis
Remember Patients with systemic autoimmune disease can have multiorgan involvement, such as pericarditis, nephritis, pleuritis, arthritis, and skin disorders.
292
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)
293
Differential diagnosis for pericarditis
Remember to differentiate pericarditis from other life-threatening causes of chest pain, including acute coronary syndrome, myocarditis or pulmonary thromboembolism
Myocardial Infarction (Acute Coronary Syndrome)
Pulmonary Embolism
Pneumonia
Pneumothorax
Costochondritis
294
Causes of Pericarditis
(CARDIAC RIND)
295
Complications of pericarditis
Pericardial effusion
Cardiac Tamponade
Chronic constrictive pericarditis
296
Symptoms similar to pericarditis
297
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
298
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.
299
What is pericardial effusion
Accumulation of fluid in the pericardial sac. May result from pericarditis.
300
What causes pericardial effusion
May result from causes of pericarditis
Hyperthyroidism also causes pericardial effusion and rarely compromises ventricular function.
Certain cancers
301
Risk Factors for pericardial effusion
Previous pericarditis
Age
Previous infections
302
Complications to pericardial effusion
Cardiac tamponade
Constricitve pericarditis
303
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
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Diagnosis of pericardial effusion
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Treatment for pericardial effusion
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What is infective endocarditis
Infection of the endocardium due to a bacterial/fungal infection of the endocardial lining of the heart valves
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What causes infective endocarditis
Firstly damage/injury to valves. Serves as a place for bacteria to adhere to
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Infective endocarditis should be suspected in individuals with..
Fever
Risk Factors of: Prosthetic valve/cardiac device, intravenous drug use, immunosuppression, dental/surgical procedure
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Diagnosis for infective endocarditis
Diagnosis confirmed according to Duke's criteria. Takes into account clinical presentation, blood cultures for microbiological data, and echocardiography
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Treatment for infective endocarditis
IV for 6 weeks
Surgical debridement
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Prevention of infective endocarditis
antibiotic prophylaxis with amoxicillin orally or ampcillin IV/IM 1 hour before procedure
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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
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Clinical Presentation of valvular disease
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Clinical auscultation of valvular disease
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What is aortic stenosis?
Characterised by the obstruction of left ventricular outflow resulting in a decrease of cardiac output
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Cardiac signs of aortic stenosis
Exertional dizziness or syncope
Exertional dyspnea
Exertional angina
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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)
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Aetiology of aortic stenosis
1.Congenital abnormal valve (unicuspid/bicuspid)
2. Calcification of tricuspid valve
3. Rheumatic valvular disease
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Investigations for aortic stenosis
ECG: may show left ventricular hypertrophy
Cardiac catheterisation
*Transthoracic echocardiogram* GOLD STANDARD
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Management for aortic stenosis
Surgical Valve replacement: mechanical, bioprosthetic
Long-term anticoagulants
Inoperable patients:
Balloon valvuloplasty
Trans catheter valve replacement
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What is aortic regurgitation
Characterised by the backflow of blood into the right atrium during systole
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Classifications of aortic regurgitation
Primary
Secondary/Functional (Most common)
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Causes of primary aortic regurgitation
+ Marfan Syndrome
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Causes of secondary/functional aortic regurgitation
*Pulmonary Hypertension
*Dilation of the tricuspid annulus
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Pathophisiology of aortic regurgitation
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Clinical examination of aortic regurgitation
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Investigations for aortic regurgitation
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Treatment for aortic regurgitation
Aside from open heart surgery trans-catheter options: annuloplasty, valve replacement, coaptation device
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What is mitral stenosis
Narrowing of the mitral valve of the heart. This leads to complications due to impairment of blood flow
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Aetiology of mitral Stenosis
Rheumatic fever leading to rheumatic heart disease (95% of cases)
Congenital
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Symptoms of mitral stenosis
Exertional dyspnoea
Decreased excercise tolerance
Haemoptysis
Chest pain
Fatigue
History of rheumatic fever
Malar flush
Signs of right-sided heart failure
ascites
raised JVP
peripheral oedema
Thromboembolic event "Stroke"
Hoarseness (recurrent laryngeal nerve compressed)
Dysphagia (esophagus compressed)
Cardiovascular Examination
Malar flush
Pulse
Weak pulse due to reduced strove volume
Atrial fibrillation
Left parasternal heave (from right ventricular hypertrophy)
Auscultation - Mitral valve (Apex - left 5th intercostal space mid-clavicular)
Pre systolic murmur precedes S1, a result of increase blood flow from atrial contraction
Opening snap of the mitral valve following S2 (closure of the aortic and pulmonic valves) is the opening of the stenotic mitral valve (SNAP)
Long murmur during Diastole (longer in chronic mitral stenosis)
Low-pitched diastolic rumble that is most prominent at the apex.
Side note Early diastolic murmur (on inspiration) due to pulmonary regurgitation from pulmonary hypertension (Graham Steell murmur) may be heard rarely.
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Risk Factors with mitral stenosis
Streptococcal infection
Ergot medications
Serotogenic medications
SLE
Amylodoisis
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Differential diagnosis of mitral stenosis
Symptoms and signs similar to mitral stenosis
left atrial myxoma
prosthetic valve obstruction
Cor tratriatum
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Investigations for mitral stenosis
ECG
Atrial fibrillation
Left atrial enlargement - P mitrale
Right ventricular hypertrophy - Right axis deviation
Chest X-ray
Straight or convex L heart border
Double shadow of LA behind RA
Splaying of carina
Dilated upper lobe veins
Prominent pulmonary conus
Pulmonary haemosiderosis
Trans-thoracic echocardiography
Transoesophageal echocardiography
Cardiac catherization
Diagnosis
Echocardiography — A transthoracic echocardiogram is indicated in patients with signs or symptoms of MS to establish the diagnosis, quantify the hemodynamic severity determine the etiology, and assess concomitant valve disease.
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Management of mitral stenosis
Medication - Preload reduction
No treatment generally required if asymptomatic but monitoring is important
Diuretics and sodium
Think ACE inhibitors have no role as the ventricles are normal
Surgery
Balloon valvotomy
moderate to severe symptomatic disease
Diuretic
Valve replacement or repair
Mechanical
Bioprosethetic
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What is mitral regurgitation
Leakage of blood backward through the mitral valve each time the left ventricle contracts
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Complications of mitral stenosis
Atrial Fibrillation
Stroke
Warfarin-induced haemorrhage
Systemic Embolism - due to thrombus formation in the right atrium
Infective endocarditis
Functional tricuspid reguritation
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Aetiology of mitral regurgitation
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Signs and symtpoms of mitral regurgitation
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Examination findings of mitral regurgitation
*Diminished S1 Heart Sounds
Flat continuous murmur in systole (pain/holosystolic murmur). Murmur radiates to left axilla
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Management of mitral regurgitation
Preoperative diuretic
Valvuloplasty
Valve Repair/Replacement
Annuloplasty
Intra-aortic balloon counterpulsation
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What is circulatory shock?
Body wide deficiency of blood supply. It causes:
-Oxygen deprivation
-Buildup of waste products
Causes eventual organ failure if untreated
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Types of shock
Hypovolaemic when circulatory blood volume is SEVERELY REDUCED
Cardiogenic is when the heart fails to pump sufficiently
Distributive results from EXCESSIVE DILATION of blood vessels decreasing bp
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Causes of hypovolemic shock
External/Internal Blood loss
Fluid Loss
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Causes of cardiogenic shock
Sudden heart attack
End-stage cardiomyopathy, valvular disease, myocarditis, cardiac arrythmias
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Causes of distributive shock
Sepsis: overhwelmed by infection, resonds with systemic cytokine release causing vasodilation and fluid leakage from capillaries
Anaphylaxis: immune system OVERREACTS to an allergen, releasing ++ histamine ...
Neurogenic: result of spinal cord injury. Damage of autonomic nervous system, sympathetic tone causing vasoconstriction is lost, causing VASODILATION & hypotension
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Signs of shock
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Physiologic change of shock
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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)
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What is cardiomyopathy
Disease of the heart muscle tissue
Heterogenous group of diseases -> Heart failure
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What are the determinants of myocardial performance
Preload: Amount of blood entering ventricles during diastole -> End Diastolic Volume
Afterload: Force ventricles must overcome
Contractility
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What are the diff types of cardiomyopathy
* Hypertrophic: left ventricular hypertrophy without chamber dilation
* Dilated : dilation and impaired contractility of 1 or both ventricles
* Restrictive
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Prevalence of hypertrophic cardiomyopathy
Prevalence 1:500
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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
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What are the two ‘types’ of hypertrophic cardiomyopathy
Obstructive type: Left ventricular hypertrophy, no chamber dilation, interventricular septal hypertrophy
Non Obstructive: Left ventricular hypertrophy
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Mechanism of disease for hypertrophic cardiomyopathy
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Clinical manifestation of hypertrophic cardiomyopathy
More pronounced symptoms when exercising: syncope, angina, dyspnea
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Investigations for hypertrophic cardiomyopathy
ECG
Echocardiagram
Cardiac MRI
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Treatment for hypertrophic cardiomyopathy
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Clinical manifestations of dilated cardiomyopathy
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
S3 Gallop
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Aetiology of dilated cardiomyopathy
Primary: Genetics inherited
Secondary: viruses & substances, coronary artery disease, valvular disease, arrhythmia
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Complications of dilated cardiomyopathy
Tricuspid Valve insufficiency
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What do you see on an echocardiogram with a patient having dilated cardiomyopathy
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Treatment for dilated cardiomyopathy
Treatment- Heart Failure
-fluid restriction
-daily weights
-diuretics
-ACEi
-Betablockers
-Spironolactone
-ICD
- Heart Transplant
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Causes of restrictive cardiomyopathy (Pneumonic: LASHER)
Loffler Syndrome
Amyloidosis
Sarcoidosis
Haemochromatosis
Endocardial fibroelastosis
Post-Radiation
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Signs and symptoms of restrictive cardiomyopathy
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Investigations for restrictive cardiomyopathy
ECG
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Treatment for restrictive cardiomyopathy
Loop Diuretics
ACEi, CCB, Betablockers
Heart Transplant
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Cardiomyopathy table
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What is rheumatic fever
Autoimmune inflammatory disease caused by complication of streptococcal infection
Develops after streptococcal pharyngitis (strep throat) from Group A beta haemolytic streptococcus
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Causes of rheumatic fever
Molecular mimicry
Pancarditis
Chronic rheumatic heart disease
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Risk factors of rheumatic fever
Strep throat (small chance)
1/3 cases asymptomatic
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Pathophisiolgy of rheumatic fever
*Genetic predisposition + interaction * with group A streptococci -> Autoimmune response
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Signs and symptoms of rheumatic fever
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Diagnosis of Rheumatic fever
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Treatment for rheumatic fever
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What is tetralogy of Fallot
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Causes of tetralogy of Fallot
Cause unclear
-chromosome 22 deletions
-DiGeorge syndrome
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Significance of tetralogy of Fallot
Most common cyanotic congenital heart defect -> 50-70%
10% All congenital heart defect
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Symptoms of Tetralogy of Fallot
Baby:
Cyanosis to lips + fingertips
Clubbing in fingers & toes
Any decrease in O2
Cyanotic Spell: relieved with squatting down
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Diagnosis of Tetralogy of Fallot
Echocardiogram: can be done prenatally
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Treatment for Tetralogy of Fallot
Cardiac repair surgery
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What is coarctation of the aorta
A narrowed segment of the aorta
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What are the 2 forms of coarctation of the aorta
Infant from: 70%, after aortic arch, before patent ductus arteriosus
Adult form: 30%, no patent ductus arteriosus, due to upstream/downstream issues
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Signs and symptoms of coarctation of aorta
Systolic murmur:
-Systole: diamond-shaped murmur
-Diastole: high-pitched decrescendo murmur
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Clinical Presentation of infant coarctation
Lower extremity cyanosis
Absent or delayed femoral pulse
BP higher in upper extremities
Often don’t survive post neonatal period
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Causes of infant coarctation
Happens during foetal development
-Often after congenital changes
-associated with Turner Syndrome
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Causes involving adult coarctation
Upstream:
-Risk of Berry aneurysm
-Risk of aortic dissection
Downstream
Hypertension
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Diagnosis of coarctation of aorta
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Treatment of coarctation of aorta
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What is patent ductus arteriosus
Ductus arteriosus remains open after birth
Left-to-right shunt between atria
Sometimes presents with congenital defects
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Causes of Patent Ductus Arteriosus
Congenital rubella
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Signs and symptoms of Patent ductus arteriosus
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Diagnosis of Patent Ductus Ateriosus
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Treatment of Patent Ductus Arteriosus
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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
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Signs and symptoms of Ventricular Septal Defect (VSD)
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Diagnosis of Ventricular Septal Defect
Echocardiogram = Gold Standard
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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
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Pathology and Causes of Atrial Septal Defect
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Signs and Symptoms of atrial septal defect
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Diagnosis of atrial Septal Defect
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Treatment of atrial Septal Defect
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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
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Types of Long QT syndrome
Types of Long QT syndrome
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Risk Factors of Long QT interval
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Complication of Long QT interval
Malignant arrhythmias, syncope, seizures, sudden death
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Diagnosis of Long QT interval
Serum electrolytes : Hypokalaemia, hypomagnesaemia, hypocalcaemia may be present
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Treatment for long QT interval
Congenital : Beta Blockers
Acquired : Magnesium sulfate, isoproterenol, lidocaine
Surgery
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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)
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Risk Factors of Torsades des Pointes
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Complications of Torsades des pointes
Ventricular fibrillation, seizures, sudden cardiac death
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Signs and symptoms of Torsades des Pointes
Palpitations. Lightheadedness, syncope
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ECG findings on Torsades des Pointes
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Treatment for Torsades des Pointes
Medications & Surgery
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S1 is caused by closure of mitral and tricuspid valves
Causes of a loud S1
mitral stenosis
left-to-right shunts
short PR interval, atrial premature beats
hyperdynamic states
Causes of a quiet S1
mitral regurgitation
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With respect to ischaemic heart disease, the key molecule that is reduced in endothelial dysfunction
Nitric oxide
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Chest X ray findings for heart failure
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Murmur
**Ejection systolic**
louder on expiration
aortic stenosis
hypertrophic obstructive cardiomyopathy
louder on inspiration
pulmonary stenosis
atrial septal defect
also: tetralogy of Fallot
**Holosystolic (pansystolic)**
mitral/tricuspid regurgitation (high-pitched and 'blowing' in character)
tricuspid regurgitation becomes louder during inspiration, unlike mitral reguritation
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole
ventricular septal defect ('harsh' in character)
**Late systolic**
mitral valve prolapse
coarctation of aorta
**Early diastolic**
aortic regurgitation (high-pitched and 'blowing' in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character)
**Mid-late diastolic**
mitral stenosis ('rumbling' in character)
Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character)
**Continuous machine-like murmur**
patent ductus arteriosus
RILE
Right-sided murmur → heard best on Inspiration
Left-sided murmur → heard best on Expiration
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What medication worsens symptoms of peripheral vascuolar disease
Beta-blockers may worsen symptoms of patients suffering from peripheral vascular disease.
