Cardiovascular Flashcards
What is sudden cardiac arrest
A sudden state of circulatory failure due to a loss of cardiac systolic function.
What are the 4 cardiac rhythm disturbances which cause cardiac arrest
Ventricular fibrillatio
Pulseless ventricular tachycardia
Pulseless electrical activity
Asystole
What is tornadoes de pointes
A sub-group of polymorphic VT in patients with an underlying prolonges QT interval, sometimes related to hypomagnesaemia
How does cardiac arrest present
Patient unresponsive
Absence of normal breathing
Absence of circulation (no pulse)
Cardiac rhythm disturbance
What are the risk factors for cardiac arrest
Strong:
-Coronary artery disease
-Left ventricular dysfunction
-Hypertrophic cardiomyopathy
-Arrhythmogenic right ventricular dysplasia
-Long QT syndrome
-Medications which prolong the QT interval or cause electrolyte disturbances
-Acute medical or surgical emergency
-Illicit substances
Weak:
-Brugada syndrome
-Valvular heart disease
-Smoking
-History of eating disorders
What are the investigations for suspected cardiac arrest
1st line:
-Continuous cardiac monitoring
-FBC
-Serum electrolytes (electrolyte imbalances, esp hyperkalaemia or hypokalaemia)
-ABG
-Cardiac biomarkers
-Point of care ultrasound
Consider also:
-ECG
-Coronary angiography
-Echocardiogram
-Chest x-ray
-Toxicology screen
-Cardiac MRI
-Signal-averaged electrocardiogram (SAECG)
-Electrophysiological study
How is a cardiac arrest managed
Basic life support:
Give naloxone in suspected opioid overdose
Give adrenaline to increase rate of achieving spontaneous circulation and to increase short term survival
In patients with sudden cardiac arrest due to torsades de pointes, giving magnesium may restore a perfusing cardiac rhythm
Assessment for and treatment of any suspected reversible causes of cardiac arrest
ACLS:
Shockable rhythms:
-Pulseless VT and VF
-BLS in community
-Give adrenaline
-If no spontaneous circulation resolves and a shockable rhythm identified, one shock should be delivered followed by 5 cycles (2 mins) of CPR
-IV or IO access obtained without interupting CPR
-Reassess pulse and rhythm, is no change then shock again along with amiodarone or lidocaine and continue CPR for 5 cycles
-Reasses, if no change restart at stage of adrenalin administration
-Continue until spontaneous circulation achieved or resus measures are terminated
Non-shockable rhythms:
-Pulseless electrical activity or asystole
-BLS
-If spontaneous circulation is not restores, and a non-shockable rhythm is identified, 5 cycle of CPR are provided
-IV or IO access is obtained without interrupting CPR
-Give adrenaline asap and every 3-5 mins after
-Check response after every 5 cycles (2 mins) of CPR
-Continue this cycle of giving CPR and adrenaline until spontaneous ciculation is attaned or resus is terminated
What post-resuscitation care can be provided in cardiac arrest
If spontaneous circulation is achieved, immediately commence post-resuscitation care:
-monitoring
-organ support
-correction of electrolyte imbalances and acidosis
-safe transfer to a critical care environment
-thorough search for potnetial aetiology
-modify/treat risk factors for sudden cardiac arrest
12 lead ECG to determine signs of STEMI and if present then emergent coronary angiography with or without PCI should be performed. In some cases can also be done in those with ACS but no sign of STEMI.
Anoxic brain injury is a frequent complication of sudden cardiac arrest and targeted temperature management protocals can be used to improve survival and neurological outcome.
What is targeted temperature management
Used in post-resuscitation from cardiac arrest.
AIm for between 32 and 36 degrees C
Three phases of Induction, Maintenance, Rewarming
Induction and/or maintenance achieved by:
-Icepacks with or without wet towels
-Cooling blankets or pads
-Water or air-circulating blankets
-Transnasal evaporative cooling
-Intravascular heat exchanger
-Extracorporeal circulation
Rewarming should be achieved slowly (0.25°C to 0.50°C of warming per hour) to avoid rebound hyperthermia, which is associated with worse neurological outcomes
When can resuscitation of a cardiac arrest be terminated
Pre-hospital guidance. Must meet all:
For BLS EMS
-EMS did not witness the arrest
-The patient had no ROSC before transport
-No shock was administered before transport
For ALS EMS:
-Arrest not witnessed
-No bystander CPR was provided
-The patient had no ROSC before transport
-No shock was administered before transport
Resuscitative measures should be terminated if there is documentation of a valid “do not resuscitate” order
Terminating resuscitative measures may also be considered on the basis of the following:
-Delayed initiation of CPR in unwitnessed cardiac arrest
-Unsuccessful resuscitation after 20 mins of ACLS guideline-directed therapy
-conditions that compromise the safety of the emergency care providers
What are the potential complications of cardiac arrest
Death
Rib and sternal fractures
Anoxic brain injury
Ischaemic liver injury (shock liver)
Renal acute tubular necrosis (ATN)
Recurrent cardiac arrest
What is the prognosis following cardiac arrest
Generally poor
Early provision of CPR, including compressiononly CPR, by bystanders during out-of-hospital arrest increases the rate of survival from sudden cardiac arrest
Even those who do survive to hospital admission do not always survive to hospital discharge and those who do survive to hospital discharge often have neurological, pulmonary, cardiac, hepatic, renal or MSK complications
What is myocardial infarction
Myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand
What is STEMI
ST-elevation myocardial infarction
Caused predominantly by complete atherothrombotic occlusion of a coronary artery
Diagnosed clinically when there is new (or increased) and persistent ST-segment elevation in at least 2 contiguous leads of ≥1 mm in all leads other than leads V2-V3 where the following cut-off points are:
- ≥2.5 mm in men <40 years old
- ≥2 mm in men >40 years old
- ≥1.5 mm in women regardless of age
(1 mm = 1 small square (at a standard ECG calibration of 10 mm/mV).)
Contiguous ECG leads lie next to each other anatomically and indicate a specific myocardial territory
How does an MI present
Common:
Chest pain
Dyspnoea
Pallor
Diaphoresis
Cardiac risk factors
Nausea and/or vomiting
Dizziness or light-headedness
Distress and anxiety
Palpitations
Uncommon:
Abnormal breath sounds
Additional heart sounds
Cardiogenic shock
Reduced consciousness
Hypotension
Atypical location or nature of pain
What is the chest pain described in MI
Central
Retrosternal, crushing, heavy, severe, and diffuse in nature
May be described by the patient as “pressing or squeezing”
May occur at rest or on activity
May be constant or intermittent, or wax and wane in intensity
Sometimes radiating to the left arm, neck or jaw
May be associated with nausea, vomiting, dyspnoea, diaphoresis, lightheadedness, palpitations or syncope
What investigations should be performed in suspected STEMI
ECG
Coronary angiography
Cardiac troponin
Glucose
FBC
U and Es
CRP
Serum lipids
Consider also:
ABG
Chest X-ray
Point of care transthoracic echocardiogram
Emerging tests:
Cardiac myosin-binding protein C (cMyC)
What are the differentials in suspected STEMI
Unstable angina
N-ST-EMI
Aortic dissection
Pulmonary embolism (PE)
Pneumothorax
Pneumonia
Pericarditis
Myocarditis
GORD
Oesophageal spasm
Costochondritis
Anxiety or panic attack
What is the criteria for acute, evolving ot recent MI
Either one of the following criteria:
-Typically rise of biomarkers of myocardail necrosis (troponin or creatine kinase-MB) with at least one of the following:
– Ischaemic symptoms
– Development of pathological Q waves on ECG
– ECG changes indicative of ischameia (ST-segment elevation or depression)
– Coronary artery intervention
-Pathological findings of acute MI
What is the criteria for established MI
Any one of the following:
-Development of pathological Q waves on serial ECGs. The patient may or may not remember previous symptoms. Biochemical markers of myocardail necrosis may have normalised, depending on the length of time that has passes since the infarct developed
-Pathological findings of healed or healing MI
-Cardiac MRI with delayed enhancement imaging showing a classic sub-endocardial or transmural infarct in a coronary artery distribution
How is STEMI managed
Give all patients with suspected acute coronary syndrome a single loading dose of aspirin as soon as possible, unless they have aspirin hypersensitivity
Make a clinical diagnosis of STEMI and start treatment if the patient has sighns and symptoms of myocardial ischaemia plus persistent/increasing ST elevation in two or more contiguous leads on ECG (do not wait for cardiac troponin to confirm)
Perform all the following in tandem as soon as a clinical diagnosis of STEMI has been made:
-Immediately assess eligibility for coronary reperfusion therapy
-For most patients the best option will be primary percutaneous coronary intervention (PCI); fibrinalysis is reserved for those without timely access to primary PCI
– if eligible, take steps to ensure reperfusion is administered asap
– If not, offer conservative medical management
-Gain IV access and start continuous haemodynamic monitoring and pulse oximetry
– Avoid cannula insertion obstructing access to the right radial artery (common entry site for primary PCI)
-Give pain relief
– IV opioid plus concomitant IV anti-emetic
-Give O2 only if sats <90%
-Give dual anthplatelt therapy by adding a P2Y12 inhibitor to aspirin
– If having PCI, use prasugrel if not already taking an oral anticoagulant, or clopidogrel if they are already taking oral anticoagulation
-Consider an IV nitrate if the patient has:
– persistent chest pain despite sublingual GTN
– Sustained hypertension
– Clinical and/or radiograpgic evidence of congestive heart failure
-Seek immediate specialist input from the interventional cardiology team
– if you are managing the patient at a non-PCI, contact the interventional cardiology team at your designated PCI-capable hospital to discuss immediate transfer
If the STEMI patient has cardiogenic shock, seek urgent senior support - coronary angiography ± PCI is indicated
When should IV nitrate not be given in STEMI
Hypotension secondary to any of:
-right ventricular infarction (usually complicating an inferior or extensive anterior STEMI)
-severe aortic stenosis or left ventricular outflow tract obstruction
-pre-existing cardiomyopathy
Persistent hypotension secondary to another cause
Use of phosphodiesterase-5 inhibitor (eg avanafil, sildenafil, tadalafil, vardenafil) for erectile dysfunction within the last 48 hours
When should and shouldn’t antivoagulant therapy be given in STEMI management
Do not give anticoagulant therapy if the patient is likely to be eligible for primary PCI
Anticoagulation will be started by the interventional cardiology team in the catheterisation lab
If the patient is having fibrinolysis, start anticoagulation at the same time. Use enoxaparin or unfractionated heparin (unless streptokinase is used for thrombolysis, in which case choose fondaparinux). Continue anticoagulation until revascularisation (if fibrinolysis is followed by PCI) or for the duration of hospital stay up to a maximum of 8 days
How should patients who have had a return of spontaneous circulation after an out of hispital cardiac arrest be managed
Primary PCI is the treatment of choice if there is STEMI on post-ROSC ECG or life-threatening arrhythmia
If no ST-segment elevation then:
- Exclude non-coronary causes of cardiac arrest
-Perform urgent Echo
-Strongly consider a referral to cardiology for urgent angiography if there is a high index of suspicion of ongoing MI despite no St-segment elevation
When deciding whether to take a survivor of cardiac arrest (with or without ST-segment elevation) to the cath lab for urgent angiography ± PCI:
- Consider each case on its individual merits and seek senior advice
- Take account of factors associated with the cardiac arrest that will influence the chance of a good neurological outcome
What is the pathophysiology of ACS
Acute coronary syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
When a thrombus forms in a fast flowing artery its is made up mostly of platelets
This is why anti-platelt medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment
What are the 3 types of ACS
Unstable angina
ST elevation myocardail infarction (STEMI)
Non-ST elevation myocardial infarction (NSTEMI)
How is suspected ACS investigated
ECG
-ST elevation or new LBBB - diagnoses of STEMI
-No ST elevation then perform troponin blood test
– If raised troponin levels and/or other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI
– If troponin levels are normal and the ECG does not show pathological changes, the diagnosis is either unstable angina or another cause such as MSK chest pain
Perform all investigation normally arranged for stable angina:
-Physical exam (heart sounds, signs of heart failure, BMI)
-ECG
-FBC (check for anaemia
-U and Es (prior to ACEi and other meds)
-LFTs (prior to statins)
-Lipid profile
-TFTs
-HbA1C and fasting glucose
Plus:
-Chest xray to investigate other causes of chest pain and pulmonary oedema
-Echo after the event to assess the functional damage
-CT coronary angiogram to assess for coronary artery disease
How does ACS present
Central, constricting chest pain associated with:
-Nausea and vomiting
-Sweating and clamminess
-Feeling of impending doom
-Shortness of breath
-Palpitations
-Pain radiating to jaw or arms
Symptoms should continue at rest for more than 20 minutes. If they settle with rest consider angina. Diabetic patients may not experience typical chest pain during an acute coronary syndrome. This is often referred to as a “silent MI”.
What are troponins
Proteins found in cardiac muscle
The specific type of troponin, the normal range and diagnostic criteria vary by lab so check policy
Diagnosis off ACS typically requires serial troponins.
A rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle
Troponins are non specific so a rise does not automatically mean ACS. Alternative causes may be:
-chronic renal failure
-sepsis
-myocarditis
-aortic dissection
-PE
What is the acute STEMI treatment
Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:
-Primary PCI (if available within 2 hours of presentation)
-Thrombolysis (if PCI not available within 2 hours)
The local cardiac centre will advise about further management (such as further loading with aspirin and ticagrelor).
WHat is PCI
Percutaneous Coronary Intervention (PCI) involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast to identify the area of blockage. This can then be treated using balloons to widen the gap or devices to remove or aspirate the blockage. Usually a stent is put in to keep the artery open.
What is thrombolysis
Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.
What is the acute NSTEMi treatment
BATMAN
B – Beta-blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)
M – Morphine titrated to control pain
A – Anticoagulant: Fondaparinux (unless high bleeding risk)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm
Give oxygen only if their oxygen saturations are dropping (i.e. <95%).
What is the GRACE score
This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:
- <5% Low Risk
- 5-10% Medium Risk
- > 10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
What are the potential complications of MI
DREAD
D – Death
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
What is Dressler’s syndrome
AKA post-myocardial infarction syndrome
Usually occurs around 2-3 weeks after an MI
Caused by a a localised immune response and causes pericarditis (inflammation of the pericardium around the heart)
Less common as the management of ACS becomes more advanced
Presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation.
Can cause a pericardial effucion and rarely a pericardial tamponade (where the fluid constricts the heart and prevents function)
A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echo (pericardial effusion) and raised inflammatory markers (CRP and ESR)
Manage with NSAIDs (aspirin/ibuprofen) and in more severe cases steroids (prednisolone)
May need pericardiocentesis to remove fluid from around the heart
What is the secondary prevention medical management for ACS
6 As
-Aspirin (75mg OD)
-Another antiplatelet (clopidogrel or ticagrelor for upto 12 months)
-Atorvastatin (80mg OD)
-ACE inhibitors (ramipril titrated as tolerated to 10mg daily)
-Atenolol (or other beta blocker titrated as high as tolerated)
-Aldosterone antagonist for those with clinical heart failure (epleretone titrated to 50mg once daily)
Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted due to higher risk of thrombus formation in different stents
What is the secondary prevention lifestyle management
Stop smoking
Reduced alcohol consumption
Mediterranean diet
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions (eg diabetes and hypertension)
What are the ECG changes in ACS
STEMI:
-ST segment elevation in leads consistent with an area of ischaemia
-New left bundle branch block
NSTEMI:
-ST segment depression in a region
-Deep T wave inversion
-Pathological q waves (suggesting a deep infarct - a late sign)
What is acute left ventricular failure
When the left ventricle is unable to adequetely move blood through the left side of the heart and out into the body.
This causes a backlog of blood that increases the amount of blood stuck in the left atrium, pulmonary veins and lungs.
The vessels in these areas are engorged with blood due to the increased colume and pressure that they leak fluid and are unable to reabsorbe fluid from the surrounding tissues, causing pulmonary oedema.
What is pulmonary oedema
Where the lung tissues and alveoli become full of interstitial fluid.
This interferes with the normal gas exchange in the lungs, causing SOB, O2 desaturation and the other signs and symptoms
What are the triggers for LVF
Iatrogenic (aggressive IV fluid in frail elderly patient with impaired left ventricular function)
Sepsis
Myocardial infarction
Arrhythmias
How does acute LVF present
Typically rapid onset breathlessness that is exacerbated by lying flat and improves on sitting up.
Causes type 1 respiratory failure (low o2 without an increase of CO2 in the blood)
SOB
Looking and feeling unwell
Cough (frothy white/pink sputum)
Increased resp rate
Reduced o2 sats
Tachycardia
3rd heart sound
Bilateral basal crackles (sound wet) on auscultation
Hypotension in severe cases (cardiogenic shock)
May also have signs and symptoms of underlying cause (chest pain, fever, palpitations)
May also have right sided heart failure (raised JVP, peripheral oedema)
How should suspected LVF be investigated
History and exam
ECG (for ischaemia and arrhythmia)
ABG
Chest Xray
Bloods:
-infection markers
-kidney function
-BNP
-troponin (if ?MI)
echo
What is BNP
B-type natriuretic peptide is a hormon that is released from the heart ventricles when the cardiac muscle (myocardium) is stretched beyond the normal range.
Finding a high result indicates the heart is overloaded (with blood) beyond its normal capacity to pump effectively
The action of BNP is to relax the smooth muscle in blood vessels. This reduces the systemic vascular resistance making it easier for the heart to pump blood through the system. It also acts on the kidneys as a diuretic to promote the excretion of more water in the urine to reduce the circulating volume helping to improve the function of the heart.
Testing for BNP is sensitive but not specific which means that when negative it is useful in ruling out hear failure, but when positive rsult can have other causes:
-Tachycardia
-Sepsis
-PE
-Renal impairment
-COPD
What is ejection fraction
Main meausure of left ventricular function
The presentage of the blood in the left ventricle which is squeezed out with each ventricular contraction
An ejection fraction above 50% is considered normal
What is cardiomegaly on chest xray
A cardiothoracic ratio of more than 50%
When the diameter of the widest part of the heart is more than half the diameter of the widest part of the lung fields
What are kerley lines
Fluid in the septal lines, seen on chest xray
How is LVF managed
Pour SOD
Pour away (stop) IV fluids
Sit up
Oxygen (if <95%)
Diuretics (IV furosemide 40mg stat)
Monitor fluid balance
IV opiates
NIV (non-invasive ventilation) (CPAP, may escalate in intubation and ventilation)
Inotropes
What do inotropes do
Strengthen the force of heart contractions and improve heart failure, but need close titration and monitoring, so need to send patient to the local coronary care unit/ HDU/ ICU)
What is hypertension
Term used to describe high blood pressure
BP >140/90 in clinic or 135/85 with ambulatory or home readings
What is essential hypertension
Accounts for 95% of hypertension
AKA primary hypertension
Means the hypertension has developed on its own and does not have a secondary cause
What are secondary causes of hypertension
ROPE
Renal disease - most common, if the bp is very high or does not respond to treatment, consider renal artery stenosis
Obesity
Pregnancy induced hypertension/ pre-eclampsia
Endocrine - most endocrine conditions can cause hypertension but primarily consider hyperaldosteronism (Conns syndrome) as this may represent 2.5% of new hypertension.
Specialist investigations should be considered in patients with a potential secondary cause for their hypertension or aged under 40 years.
What is the restfor hyperaldosteronism
Renin:akdosterone ratio blood test
What are potential complications of hypertension
Ischaemic heart disease
Cerebrovascular accident (stroke or haemorrhage)
Hypertensive retinopathy
Hypertensive nephropathy
Heart failure
How should patients be screened for hypertension
Measure BP every 5 years to screen for hypertension
It should be measured more often in those on the borderline for diagnoses
Measure every year in patients with type 2 diabetes
How is hypertension diagnosed
Patients with a clinic bp between 140/90 and 180/120 should have 24 hour ambulatory blood pressure or home readings to confirm the diagnosis, due to white coat syndrome
Measure BP in both arms and if the difference is more than 15, use the reading from the arm with higher pressure
What are the stages of hypertension
Stage 1: >140/90 (clinic) or >135/85 (Home)
Stage 2: >160/100 (clinic) or >150/95 (home)
Stage 3: >180/20 (clinic)
What tests should be performed in all patients with new diagnosis hypertension
Urine albumin: creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
Bloods for HbA1c, renal function and lipids
Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities
What are the medications used in hypertension
A – ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily)
ARB – Angiotensin II receptor blocker (e.g. candesartan 8mg to up 32mg once daily). Used in place of an ACE inhibitor if the person does not tolerate ACE inhibitors (commonly due to a dry cough) or the patient is black of African or African-Caribbean descent. ACE inhibitors and ARBs are not used together.
B – Beta blocker (e.g. bisoprolol 5mg up to 20mg once daily)
C – Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)
D – Thiazide-like diuretic (e.g. indapamide 2.5mg once daily)
How is hypertension managed
Diagnosis
Investigate for possible causes and end organ damage
Advise on lifestyle modifications
Medical management:
- all patients with stage 2 hypertension
- all patients under 80 y/o with stage 1 hypertension that also have a q risk score of 10% or more, diabetes, renal disease, cardiovascular disease or end organ damage
Step 1:
-Age <55 and non black use A
-Age over 55 or black of african or African-caribbean descent use C
Step 2:
-A and C
-Alternatively A and D or C and D
-If black then use ARB instead of A
Step 3:
-A and C and D
Step 4:
-A and C and D and additional
Additional
-if serum potassium = 4.5 mmol/l consider a potassium sparing diuretic (spironolactone)
-if serum potassium <4.5mmol/l consider an alpha blocker (doxazocin) or a beta blocker (atenolol)
Regularly check U and Es when using ACE inhibitors and all diuretics because:
-spironolactone increases risk of hyperkalaemia
-ACE inhibitors increase risk of hyperkalaemia
-Thiazide diuretics can cause hypokalaemia and other electrolyte imbalances
What is spirononlactone
A potassium sparing diuretic
Blocks the action of aldosterone in the kidneys resulting in sodium excretion and potassium reabsorption
Can be helpful to use when thiazide diuretics are causing hypokalaemia
What are the treatment targets in hypertension
<80 y/o:
-systolic <140
-diastolic <90
> 80y/o:
-systolic <150
-diastolic <90
What are the causes of chronic heart failure
Caused by either impaired left ventricular contraction (systolic heart failure) or left centricular relaxation (diastolic heart failure)
This impared left ventricular function results in a chronic back-pressure of blood trying to flow into and through the left side of the heart
How does chronic heart failure present
Breathlessness worsened by exertion
Cough (frothy white/pink sputum
Orthopnoea (SOB when lying flat, relieved by sitting or standing)
Paroxysmal nocturnal dyspnoea
Peripheral oedema
What is paroxysmal noctornal dyspnoea
Term used to describe the experience that patients have of suddenly waking at night with a severe attack of SOB and cough and maybe wheeze. Feels like they are suffocating and will sit on side of bed, or pace room or open window for air. Symptoms will improve over several minutes
What is believed to cause paroxysmal nocturnal dyspnoea
- fluid settling across a large surface of the lungs when lying flat which improves when stood up as fluid sinks to bases, clearing upper lungs
- During sleep the respiratory centre in brain is less rsponsive to resp rate and effort does not increase in response to reduced O2 sats like it normally would when awake, allowing the person to develop more significant pulmonary congestion and hypoxia before waking
- Less adrenalin circulating when sleeping, meaning the myocardium is more relaxed which worsens the cardiac output
How is chronic heart failure diagnosed
Clinical presentation
BNP blood test (NT-proBNP> 2000 warrants urgent referral)
Echo
ECG
What are the causes of chronic heart failure
Ischaemic heart disease
Valvular heart disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly AF)
How is chronic cardiac failure managed medically
ABAL
ACE inhibitor (ramilpril to 10mg OD)
Beta blocker (bisoprolol to 10mg OD)
Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or epleretone)
Loop diuretics to improve symptoms (furosemide 40mg OD)
An ARB can be used instead of ACE inhibitor if ACEi not tolerated (eg candesartan up to 32mg OD)
Avoid ACEi in patients with valvular heart disease until seen by specialist
Aldosterone antagonists are used when there is a reduced ejection fraction and symptoms are not controlled with ACEi and BB
Monitor U and Es whilst on diuretics, ACEi and aldosterone antagonists as all can causes electrolyte disturbance
What is venous thromboembolism
A common and potentially fatal condition
It involves blood clots (thrombi) developing in the circulation
Usually secondary to stagnation of blood and hypercoagulable states
What is a DVT
When a thrombus develops in the venous circulation
What is a PE
Pulmonary embolism
Once a thrombus has developed, it can embolise from the deep veins, through the right side of the heart and into the lungs where it becomes lodge in the pulmonary arteries.
This blocks blood flow to the areas of the lungs, which is when it is called a pulmonary embolism
If a patient has a hole in their heart too (eg atrial septal defect) then the blood clot can pass through to the left side of the heart and into the systemic circulation. If it travels to the brain, it can cause a large stroke
What are the risk factors of VTE
Immobility
Recent surgery
Long haul travel
Pregnancy
Hormone therapy with oestrogen (COCP and HRT)
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia
What are the throbophilias
Conditions that predispose patients to develop blood clots
Examples:
-Antiphospholipid syndrome
-Factor V Leiden
-Antithrombin deficiency
-Protein c or s deficiency
-Hyperhomocysteinaemia
-Prothrombin gene variant
-Activated protein C resistance
When should a patient be put on VTE prophylaxis and how
Every patient admitted to hospital should be assessed for their risk of VTE.
If at increased risk of VTE, they should recieve prophylaxis unless contraindicated (eg active bleeding or existing anticoagulation with warfarin or a DOAC)
Prophylaxis is usually with LMWH such as enoxaparin
Anti-embolic compression stockings are also used, unless contraindicated (eg if significant peripheral arterial disease)
How does a DVT present
Almost always unilateral; bilateral DVT is rare and bilateral symptoms are more likely due to an alternative diagnosis such as chronic venous insufficiency or heart failure.
DVTs can present with:
-calf or leg swelling
-dilated superficial veins
-tenderness to the calf (particularly over the site of the deep veins)
-oedema
-colour changes to the leg
Examine for leg swelling:
-measure the circumference of the calf 10cm below the tibial tuberosity.
-more than 3cm difference between the calves is significant
Always ask questions and examine with the suspicion of a potential PE as well.
How is D-dimer used in DVT diagnosis
D-dimer blood test is sensitive but not specific for VTE.
It is helpful in excluding VTE where there is low suspicion
It is almost always raised in DVT, but other conditions can also cause a raised d-dimer:
-pneumonia
-malignancy
-heart failure
-surgery
-pregnancy
How is DVT diagnosed
D-dimer
Doppler ultrasound of the leg - repeat negative US after 6-9 days of a positive D-dimer and the Wells score suggest a DVT likely
How is PE diagnosed
CT pulmanry angiogram (CTPA) or ventilation-perfusion (VQ) scan.
CTPA is usually preferred, unless the patient has significant kidney impairment or contrast allergy
How is VTE managed initially
Anticoagilation:
- Immediately when suspected DVT or PE (even before scan if delay)
- Usually treatment dose apixaban or rivaroxaban
- Consider catheter-directed thrombolysis in patients with a symptomatic iliofemoral DVT and symptoms lasting less than 14 days. Which involves inserting a catheter under x-ray guidance through the venous system to apply thrombolysis directly into the clot
What are the options for long term anticoagulation in VTE
DOACs, warfarin or LMWH
DOACs are oral anticoagulants that do not require monitoring.
Previously called NOACs
Options are:
-apixaban
-rivaroxaban
-edoxaban
-dabigataran
They are suitable for most patients inclusing those with cancer
Warfarin is a vitamin K antagonist.
The target INR for warfarin is between 2 and 3 when treating DVTs and PEs.
It is the first-line in patients with antiphospholipid syndrome (who also require initial concurrent treatment with LMWH)
LMWH is the first line anticoagulant in pregnancy
Continue anticoagulation for:
-3 months if there is a reversible cause (then review)
-Beyond 3 months if the cause is unclear, there is recurrent VTW or there is an irreversible underlying cause such as thrombophilia (often 6 months in practice)
-3-6 months in active cancer (then review)
What is an inferior vena cava filter
Devices inserted into the inferior vena cava, designed to filter the blood and catch any blood clots travelling through the venous system, towards the heart and lungs.
They act as a sieve, allowing blood to flow through but stopping larger blood clots.
Used in unusual cases of patients with reccurrent REs or those that are uunsuitable for anticoagulation
How are unprovoked DVTs investigated
When patients have their first VTE without clear cause:
-review medical history
-baseline bloods
-physical exam for evidence of cancer
In those who have had unprovoked VTE and are due to finish their anticoagulation, test for:
-antiphospholipid syndrome (check antiphospholipid antibodies)
-hereditary thrombophilias (only is they have 1st degree relative also affected by a DVT or PE)
What is peripheral arterial disease
Refers to the narrowing of the arteries supplying the limbs and periphery, reducing the blood supply to these areas
Usually refers to lower limbs, resulting in symptoms of claudication
What is intermittent claudication
A symptom of ischaemia in a limb, occurring during exertion and relieved by rest.
Peripheral arterial presents with this.
Typically a crampy, achy pain in the calf, thigh or buttock muscles, associated with muscle fatigue when walking beyond a certain intensity
What is critical limb ischameia
The end-stage of peripheral arterial disease, where there is inadequate supply of blood to a limb to allow it to function normally at rest.
The features are pain at rest, non-healing ulcers and gangrene.
There is a significant risk of losing the limb.
What is acute limb ischaemia
Refers to a rapid onset of ischaemia in a limb
Typically due to a thrombus, clot, blocking the arterial supply of a distal limb, similar to a thrombus blocking a coronary artery in MI
What is ischaemia
An inadequate oxygen supply to the tissues due to reduced blood supply
What is necrosis
Death of tissue
What is gangrene
The death of the tissue, specifically due to an inadequate blood supply
What is atherosclerosis
A combination of atheromas (fatty deposits in the artery walls) and sclerosis (the process of hardening and stiffening of the blood vessel walls)
It affects the medium and large arteries
It is caused by chronic inflammation and activation of the immune system in the artery wall
Lipids are deposited in the artery wall, followed by the development of fibrous atheromatous plaques
What do atheromatous plaques cause
Stiffening of the artery walls, leading to hypertension and strain on the heart (whilst trying to pump blood against increased resistance
Stenosis, leading to reduced blood flow (eg in angina)
Plaque rupture, resulting in a thrombus that can block a distal vessel and cause ischaemia (eg in acute coronary syndrome)
What are the risk factors for atherosclerosis
Non-modifiable:
-Old age
-FH
-Male
Modifiable:
-Smoking
-Alcohol consumption
-Poor diet (high in sugar and trans fat and low in fruit, veg and omega 3s)
-Low exercise/ sedentary lifestyle
-Obesity
-Poor sleep
-Stress
Which medical comorbidities increase the risk of atherosclerosis
Diabetes
Hypertension
CKD
Inflammation conditions eg rheumatoid arthritis
Atypical antipsychotic medications
What are the potential end results of atherosclerosis
Angina
MI
TIA
Stroke
Peripheral arterial disease
Chronic mesenteric ischaemia
What are the features of critical limb ischaemia (6 P’s)
Pain (burning pain worse at night when leg raised as gravity does not help pull blood into the foot)
Pallor
Pulseless
Paralysis
Paraesthesia (abnormal sensation or pins and needles)
Perishing cold
What is Leriche Syndrome
Leriche Syndrome occurs with occlusion in the distal aorta or proximal common iliac artery
There is a clinical triad of:
-Thigh/buttock claudication
-Absent femoral pulses
-Male impotence
What are the signs of peripheral arterial disease on examination
Look for risk factors:
-Tar staining on the fingers
-Xanthoma (yellow cholesterol deposits on the skin)
Look for signs of cardiovascular disease:
-Missing limbs or digits after previous amputations
-Midline sternotomy scar (previous CABG)
-A scar on the inner calf for saphenous vein harvesting (previous CABG)
-Focal weakness suggestive of previous stroke
Peripheral pulses may be weak on palpation, can use hand-help doppler to accurately assess difficult pulses
Signs of PAD on inspection:
-Skin pallor
-Cyanosis
-Dependent rubor (a deep red colour when the limb is lower than the rest of the body)
-Muscle wasting
-Hair loss
-Ulcers
-Poor wound healing
-Gangrene (breakdown of skin and a dark red/black change in colouration
-Reduced skin temp
-Reduced sensation
-Prolonged cap refill
-Changes during Buerger’s test
What is Buerger’s test
Buerger’s test is used to assess for peripheral arterial disease in the leg. There are two parts to the test.
The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease. Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply. For example, a Buerger’s angle of 30 degrees means that the legs go pale when lifted to 30 degrees.
The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go:
Blue initially, as the ischaemic tissue deoxygenates the blood
Dark red after a short time, due to vasodilation in response to the waste products of anaerobic respiration
The dark red colour is referred to as rubor.
What are arterial leg ulcers
Leg ulcers indicate the skin and tissues are struggling to heal due to impaired blood flow
Two types:
-arterial and venous
What are arterial ulcers
Caused by ischaemia secondary to an inadequate blood supply
Smaller than venous
Deeper than venous
Well defined borders
Punched out appearance
Occur peripherally (eg toes)
Reduced bleeding
Painful
What are venous ulcers
Caused by imparied drainage and pooling in the legs
Occur after a minor injury to the legs
Larger than arterial
More superficial than arterial
Irregular, gently sloping borders
Affect the gaiter area of the leg (mid calf down to the ankle)
Less painful than arterial
Occur with other signs of chronic venous insufficiency (eg haemosiderin stainging and venous eczema)
What investigations should be performed in suspected peripheral arterial disease
Ankle brachial pressure index (ABPI)
Duplex ultrasound (shows the speed and volume of blood flow)
Angiography (CT or MRI) (using contrast to highlight the arterial claudication
What is ABPI
Ankle brachial pressure index is the ratio of systolic blood pressure in the ankle (around lower calf) compared with the systolic blood pressure in the arm
The readings are taken manually using a Doppler probe
Results:
->1.3 can indicate calcification of the arteries, making them difficult to compress (often diabetic)
-0.9-1.3 is normal
-0.6-0.9 indicates mild peripheral arterial disease
-0.3-0.6 indicates moderate peripheral arterial disease
-Less than 0.3 indicates severe disese to critical ischaemic
How is intermittent claudication managed
Lifestyle changes
Optimise medical treatment of comorbidities
Exercise training to push near maximal claudication and pain, then rest and repeat
Medical treatment:
-atorvastatin 80mg
-clopidogrel 75mh OD (aspirin second line)
-Naftidrofuryl oxalate (5-Ht2 receptor antagonist that acts as a peripheral vasodilator)
Surgical:
-Endovascular angioplasty and stenting
-Endarterectomy (cutting vessel open to remove athermatous plaque)
-Bypass surgery (using a graft to bypass the blockage)
What is endovascular angioplasty and stenting
Involves inserting a catheter through the arterial system under X ray guidance
At the site of the stenosis a balloon is inflated to create space in the lumen
A stent is inserted to keep the artery open
Lower risk treatment but might not be suitable for more extensive disease
How is critical limb ischaemia managed
Require urgent referral to the vascular team
Analgesia
Urgent revascularisation can be achieved by:
-Endovascular angioplasty and stenting
-Endarterectomy
-Bypass surgery
-Amputation of the limb if it is not possible to restore the blood supply
How acute limb ischaemia managed
Require urgent referral to the oncall vascular team for assessment
Management options:
-Endovascular thrombolysis- inserting a catheter through the arterial system to apply thrombolysis directly into the clot
-Endovascular thrombectomy- inserting a catheter through arterial system and removing the thrombus by aspiration or mechanical devices
-Surgical thrombectomy- cutting open the vessel and removing the thrombus
-Endarterectomy
-Bypass surgery
-Amputation if necessary
What is superficial vein thrombosis
AKA Superficial thrombophlebitis
Results from thrombus formation in a superficial vein, with associated inflammation in the tissue surrounding the vein
Where is the most common site of serficial veing thrombosis
Saphenous vein and its tributaries of the lower limbs (60-80% of cases)
Superficial veins in other areas of the body can be affected (upper limbs, neck, abdominal wall, breast, arms)
What is migratory thrombophlebitis
Thrombophlebitis that recurs at varying sites but most commonly in the leg
Often associated with a serious underlying cause (eg cancer)
What is Trousseau syndrome
A rare condition characterised by recurrent and migratory superficial vein thrombosis, frequently in unusual sites, such as arm or chest (AKA Mondor’s disease when involving chest wall veins)
Most often associated with gliomas and adenocarcinomas of the GI tract (stomach, pancreas and colon), lungs, breast, ovaries and prostate
Can also be seen with Behcet’s and Buerger’s disease
What causes superficial vein thrombosis
Often associated with prothrombotic conditions characterised by one or more of the components of Virchow triad resulting in thrombus formation
Risk:
-Varicose veins are most common risk factor for the lower legs
-Thrombophilia
-Autoimmune disease (Behcet’s and Buerger’s)
-Previous history of it
-IV injections or cannulation
-Cancer
-Pregnancy and up to 6 weeks post fatally
-Female
-Older age
-Prolonged immobilisation
-Oral contraceptives or HRT
-Obesity
What is Virchow triad
Vessel wall damage
Venous stasis
Hypercoagulability of blood
How is superficial vein thrombosis assessed
History:
-Symptom duration and severity
-Pain, tenderness, itching, reddening of the skin, hardening of surrounding tissue
-Pigmentation changes
-Typically develop over hours to days and resolve in days to weeks, but hardness may persist longer
-Identify risk factors
Exam:
-Look for varicose veins and other signs of venous insufficiency
-Examine standing and lying
-In those with pre existing varicose veins: Tender worm like mass deep to the skin with overlying skin warm and erythematous, often with oedemaof the surrounding area without swelling of the whole limb
-In those without varicose veins: often a palpable cord, sometimes nodular, associated with warmth, tenderness and erythema along the course of a non-varicose superficial vein
Assess for DVT or PE
Assess for complications:
-Infection
Suspect migratory superficial thrombophlebitis if a person has repeated thromboses developing in superficial veins at varying sites
Consider differentials in atypical presentations
What are the differentials in superficial vein thrombosis
DVT
Cellulitis
Chronic venous insufficiency
Insect bite or stings
Lymphangitis
Tendonitis
Vasculitic conditions (eg erythema nodosum and polyarteritis nodosum)
How is superficial vein thrombosis treated
Analgesia
Warm compress and elevation
Only give antibiotics if signs of infection
Consider referral to vascular service for venous duplex scanning to guide treatment and need for further specialist intervention:
-LMWH and fondaparinux to reduce risk of extension and recurrence
-Fondaparinux significantly reduces risk of symptomatic venous thromboembolism and may be considered in those of increased risk of DVT or PE
Compression sticking after excluding arterial insufficiency
Provide written information on the condition
What are the potential complications of superficial vein thrombosis
DVT or PE
Infection
Skin changes
Varicose veins
