Cardiovascular system Flashcards
Atherosclerosis DR DEAC PIMP
D: Arteriosclerosis: arterial wall thickening (hardening) and elasticity loss with variable pathogenesis
Atherosclerosis (most common type of arteriosclerosis)
Multifactorial inflammatory disease of the intima, manifesting at points of hemodynamic shear stress
Characterized by a build-up of cholesterol plaques in the intima
Affects elastic arteries and large/medium-sized muscular arteries
R: Modifiable risk factors Smoking Diabetes mellitus Arterial hypertension Dyslipidemia High homocysteine levels (homocystinuria) Obesity High fibrinogen levels Hyperphosphatemia Stress Increased alcohol consumption Nonmodifiable risk factors Family history: cardiovascular events in first-degree relatives below the age of 55 (♂)/65 (♀) Age: males ≥ 45 years, females ≥ 55 years (postmenopause).
D: Aneurysm. Weakening of vessel wall: arterial aneurysm or dissection
Demand-supply mismatch: coronary heart disease (CHD), peripheral artery disease (PAD), intestinal ischemia, and subcortical vascular dementia (Binswanger disease)
Thrombosis and thromboembolism: acute coronary syndrome, stroke
Renovascular hypertension: atherosclerosis of the renal artery → activation of the renin-angiotensin-aldosterone system
E: Leading cause of vascular disease worldwide
Sex: ♂ > ♀
A:
C:
P: Pathogenesis of atherosclerosis
Chronic stress on the endothelium
Endothelial dysfunction, which leads to
Invasion of inflammatory cells (mainly monocytes and lymphocytes) through the disrupted endothelial barrier
Adhesion of platelets to the damaged vessel wall → platelets release inflammatory mediators (e.g., cytokines) and platelet-derived growth factor (PDGF)
PDGF stimulates migration and proliferation of smooth muscle cells (SMC) in the tunica intima and mediates differentiation of fibroblasts into myofibroblasts
Inflammation of the vessel wall
Macrophages and SMCs ingest cholesterol from oxidized LDL and transform into foam cells.
Foam cells accumulate to form fatty streaks (early atherosclerotic lesions).
Lipid-laden macrophages and SMCs produce extracellular matrix (e.g., collagen) → development of a fibrous plaque (atheroma)
Inflammatory cells in the atheroma (e.g., macrophages) secrete matrix metalloproteinases → weakening of the fibrous cap of the plaque due to the breakdown of extracellular matrix → minor stress ruptures the fibrous cap
Calcification of the intima (the amount and pattern of calcification affect the risk of complications) [11][12]
Plaque rupture → exposure of thrombogenic material (e.g., collagen) → thrombus formation with vascular occlusion or spreading of thrombogenic material.
Common sites (in order of increasing frequency)
Circle of Willis
Carotid arteries
Popliteal arteries
Coronary arteries
Abdominal aorta
Prevention: Lifestyle modifications Weight reduction Dietary modification Moderate aerobic exercise Smoking cessation Moderate consumption of alcohol (about 1–2 glasses of wine or beer per day) presumably has a protective effect. Medical treatment: Treat hypertension, diabetes and hyperlipidemia
Hypovolemic shock Dr Deac Pimp
D:
R:
D:
E:
A: Hemorrhage
Blunt/penetrating trauma (e.g., pelvic ring/femur fractures)
Upper GI bleeding (e.g., variceal bleeding)
Postpartum hemorrhage
Ruptured aneurysm or hematoma
Arteriovenous fistula
Nonhemorrhagic fluid loss
GI loss: diarrhea, vomiting
Increased insensible fluid loss (e.g., burns, Stevens-Johnson syndrome)
Third space fluid loss (e.g., bowel obstruction)
Renal fluid loss (e.g., adrenal insufficiency, drug-induced diuresis).
C: Clinical features
Weak pulse, tachycardia, tachypnea
Hypotension
Physical examination might show:
Cold, clammy extremities, slow capillary refill
Decreased skin turgor, dry mucous membranes
Nondistended jugular veins
Findings related to the underlying disease: e.g., bleeding, melena, hematemesis, diarrhea
P: loss of intravascular fluid volume → ↓ CO and PCWP → compensatory ↑ SVR
I: Imaging to identify the underlying cause such as:
X-ray: pelvic ring fractures, hematothorax
FAST scan: intra-abdominal hemorrhage
↓ Hemoglobin and hematocrit (can be normal initially )
Pulmonary artery catheterization
↓ PCWP (< 15 mmHg)
↓ CO
↑ SVR
M: Fluid resuscitation
In the case of hemorrhage
Hemostasis
Possibly blood transfusion in a 3:1 (fluid-to-blood) ratio.
P: acute renal failure.
Abdominal aortic aneurysm
D: Localized dilation of all three layers of the abdominal aortic wall (intima, media, and adventitia) to ≥ 3 cm [1]
D: Abdominal aortic aneurysm vs thoracic aortic aneurysm.
Abdominal: location is below renal arteries (most common). Epidemiology: advanced age, predominantly men, more common than TAA.
RF is smoking (most important risk factors), atherosclerosis, hypercholesterolemia and arterial hypertension. Clinical features include pulsatile abdominal mass, bruit on auscultation, lower back pain. Diagnostics include abdominal U/S bUT FOR THORACIC:
Location is ascending aorta (most common). RF is advanced age, predominantly men. Aetiology is Arterial hypertension
Bicuspid aortic valve
Tertiary syphilis [9]
Connective tissue diseases (e.g., Marfan syndrome, Ehlers-Danlos syndrome)
Trauma
Smoking. clinical features are feeling pressure in chest and thoracic back pain. need chest x-ray and cta of chest.
E: Peak incidence: 60–70 years (rare in patients < 50 years)
Sex: ♂ > ♀: ∼ 2:1
A: Risk factors Advanced age Smoking (most important risk factor) Atherosclerosis Hypercholesterolemia and arterial hypertension Positive family history Trauma Localization Infrarenal: below the renal arteries Most common location [2] One-third of aneurysms extend into the iliac arteries. Suprarenal: above the renal arteries Shape Saccular (spherical) [3] Fusiform (spindle-shaped)
P: Inflammation and proteolytic degeneration of connective tissue proteins (e.g., collagen and elastin and/or smooth muscle cells) in high-risk patients → loss of structural integrity of the aortic wall → widening of the vessel → mechanical stress (e.g., high blood pressure) acts on weakened wall tissue → dilation and rupture may occur.
The aneurysmatic dilatation of the vessel wall may cause disruption of the laminar blood flow and turbulence.
Possible formation of thrombi in the aneurysm → peripheral thromboembolism.
C: Aortic aneurysms are usually asymptomatic or have nonspecific symptoms. They are often discovered incidentally on ultrasound or CT scan. Rupture or dissection of the aneurysm is a life-threatening condition (see “Ruptured AAA”).
Lower back pain
Pulsatile abdominal mass at or above the level of the umbilicus
Bruit on auscultation
Peripheral thrombosis and distal atheroembolic phenomena (e.g., blue toe syndrome and livedo reticularis)
Decreased ankle brachial index.
I: The diagnosis of AAA is confirmed by imaging showing aortic diameter > 3 cm. Unstable patients should be taken directly to the OR for emergency surgery if ruptured AAA is suspected (see ruptured AAA). There are no laboratory findings specific to AAA.
Imaging
Duplex ultrasound
Indications
Best initial and confirmatory test in:
Asymptomatic patients
Patients with abdominal pain and no known AAA or risk factors for AAA
To determine the presence, size, and extent of an aneurysm
Screening and surveillance
Supportive findings
Dilatation of the aorta ≥ 3 cm.
Thrombus may be present
CT angiography abdomen and pelvis with IV contrast
Indications
Imaging modality of choice in symptomatic patients and for preintervention planning
To help confirm the diagnosis when ultrasound is not possible in asymptomatic patients
More detailed evaluation of the location, size, and extent of the aneurysm, involvement of branch vessels, and presence of thrombus or rupture
Supportive findings
Dilatation of the aorta ≥ 3 cm and possibly branch vessels
Thrombus may also be present
M: Unstable patients (e.g., in case of rupture): emergency repair within 90 minutes (see “Ruptured AAA”)
Symptomatic patients with impending rupture or leaking AAA: urgent aneurysm repair within hours
Asymptomatic patients: elective aneurysm repair or aneurysm surveillance
All patients: reduction of cardiovascular risk factors [1]
Appropriate medical management of other atherosclerotic risk factors (e.g., hypertension, diabetes, hyperlipidemia)
Smoking cessation.
Invasive treatment: AAA repair
Indications [1]
Emergency repair: unstable patients
Urgent repair: impending rupture or leaking AAA
Elective repair
Fusiform aneurysm with maximum diameter ≥ 5.5 cm and low or acceptable surgical risk
Small fusiform aneurysm expanding ≥ 1 cm per year
Saccular aneurysm [1]
Aneurysm with maximum diameter 5.0–5.4 cm in women
Small aneurysm (4.0–5.4 cm) in patients requiring chemotherapy, radiotherapy, solid organ transplantation: individual approach
Procedures:
-Endovascular aneurysm repair (EVAR)
Indications: minimally invasive procedure that is preferred over open surgical repair for most aneurysms, especially in patients with a high operative risk
Procedure: Under fluoroscopic guidance, an expandable stent graft is placed via the femoral or iliac arteries intraluminally at the site of the aneurysm.
-Open surgical repair (OSR)
Indications
Mycotic aneurysm or infected graft
Persistent endoleak and aneurysm sac growth following EVAR
Anatomical contraindications for EVAR
Procedure: A laparotomy is performed and the dilated segment of the aorta is replaced with a tube graft or Y-prosthesis (bifurcated synthetic stent graft).
-Conservative treatment: AAA surveillance without repair
Small (< 5.5 cm), asymptomatic AAA can typically be observed with interval surveillance ultrasound. [12]
To identify the expansion rate and thus decrease the risk of rupture
Frequency depends on the size of the aneurysm.
P: Prognosis: 2.5-2.9cm: repeat ultrasound for 10 years. 3.0-3.9cm: us every 3 years.
4-4.9cm: US every 12 months.
5.0-5.4 cm: US every 6 months. Regular monitoring is essential because aneurysm size and expansion rate are strong predictors for the risk of rupture.
Complications:
Abdominal aortic aneurysm rupture
Embolism: caused by thrombotic material from the aneurysm
Aortic dissection
Postoperative complications [13]
Ischemia of the bowel, kidneys, and spinal cord
Anterior spinal artery occlusion
Prosthetic graft infection
Aortoenteric fistula
Complications following EVAR [1]
Endoleak
Access site complications, e.g., bleeding, hematoma, false aneurysm
Graft limb thrombosis.
Prevention: Eating nuts, fruits, and vegetables more than three times a week
Exercising more than once a week
Smoking cessation
AAA rupture
Risk factors 7.73 x increased risk in those aged >75. Family history: x8 increased risk if affected sibling. 0.7-1.5% prevalence in screened women. Smoking: OR>7 for smokers vs non-smokers. Hypertension OR 1.5 in patients with hypertension Ethnicity 50% decreased risk in black men 90% decreased risk in Asian men High cholesterol Genetic disorders Connective tissue disorders Infective (inflammatory causes)
Rapidly expanding aneurysm
Large diameter aneurysm
Smoking, tobacco use
Clinical features
Hypovolemic shock (especially in free ruptures)
Sudden onset of severe, tearing back or abdominal pain with radiation to the flank, buttocks, legs, or groin
Painful pulsatile mass
Grey Turner sign and/or Cullen sign (if there is an extensive retroperitoneal hematoma)
Nausea, vomiting
Syncope
Hematuria
Diagnostics [1]
Ruptured AAA is a clinical diagnosis; consider imaging only if the diagnosis is uncertain and the patient is hemodynamically stable
Ultrasound
Dilatation of the aorta ≥ 3 cm
Periaortic fluid
Free intra- or retroperitoneal fluid (depending on location of rupture)
CT angiography abdomen and pelvis with IV contrast: only indicated if an alternative diagnosis seems more likely
Sign of impending rupture: high-attenuation crescent within mural thrombus [14]
Signs of rupture: retroperitoneal hematoma, retroperitoneal stranding, indistinct aortic wall, extravasation of contrast
Laboratory findings that may be seen:
CBC: ↓ hemoglobin, ↓ hematocrit, ↓ red blood cell count
Metabolic acidosis in cases of shock
Treatment: emergency EVAR or OSR [1]
Prognosis: high mortality rate (∼ 81%).
The risk of rupture increases with the diameter of aneurysm (roughly 5% for 5cm aneurysm, 40% for 8 cm aneurysm). Ruptured AAA is very dangerous and has an extremely high mortality (>75%).
Presentation:
Known AAA or pulsatile mass in abdomen Severe abdominal pain (non- specific, possibly radiating to the back or loin) Haemodynamic instability (hypotension, tachycardia) Patients with suspected AAA that are haemodynamically unstable should be transferred directly to theatre from A&E resus. As the mortality is so high, transfer to theatre for surgical repair should not be delayed by getting imaging.
Diagnosis of the rupture can be confirmed or excluded by immediate CT abdomen in patients that are haemodynamically stable.
In patients that have co-morbidities that make the prognosis with surgery very poor, a discussion needs to be had with senior doctors, the patient and their family about palliative care.
Thoracic aorta aneurysm
D: Dilatation of all three layers of the aortic wall (intima, media, and adventitia) to > 150% of the normal diameter (a true aneurysm) [1]
Ascending aorta: approx. > 5.0 cm
Descending aorta: approx. > 4.0 cm
R: Risk factors
Smoking
Advanced age
Arterial hypertension
Trauma
Tertiary syphilis (due to obliterative endarteritis of the vasa vasorum) [4]
Connective tissue diseases (e.g., Marfan syndrome, Ehlers-Danlos syndrome)
Bicuspid aortic valve [5]
Positive family history
Rare: vasculitis/infectious diseases with aortic involvement (e.g., Takayasu arteritis)
D: Differential diagnoses of chest pain
See “Abdominal vs. thoracic aortic aneurysm.”
E: Less common than abdominal aortic aneurysm (AAA)
Peak incidence: 60–65 years
Sex: ♂ > ♀ (∼ 3:1)
A:
C: Aortic aneurysms are mostly asymptomatic or have nonspecific symptoms. They are often disovered incidentally on imaging.
Chest pressure
Thoracic back pain
Features of mediastinal compression/obstruction, such as:
Difficulty swallowing (esophagus)
Upper venous congestion (superior vena cava syndrome)
Hoarseness (recurrent laryngeal nerve)
Cough, wheeze, stridor (trachea)
Horner syndrome (sympathetic trunk).
P: Ascending thoracic aortic aneurysm: most often due to cystic medial necrosis
Descending thoracic aortic aneurysm: typically a result of atherosclerosis
Inflammation and proteolytic degeneration of connective tissue proteins and/or smooth muscle cells in high-risk patients → loss of structural integrity of the aortic wall → widening of the vessel
The aneurysmatic dilatation of the vessel wall may cause disruption of the laminar blood flow and turbulence.
Possible formation of thrombi in the aneurysm → peripheral thromboembolism.
I: Chest x-ray
Indications: may be conducted as an initial imaging study in patients with chest pain and/or dyspnea
Suggestive findings
Abnormal aortic contour
Widened mediastinum
Tracheal deviation
CT angiography chest
Indications: best confirmatory test for TAAs
Abnormal findings on chest x-ray, ultrasound, or echocardiography
Interventional planning and follow-up
Detailed evaluation of the extent, length, angulation, and diameter of the aneurysm
Evaluation of aortic branch involvement
Supportive findings [14][15]
Dilatation of the aorta [13]
Possible mural thrombus (nonenhancing)
Possible dissection, perforation, or rupture.
Additional imaging
MR angiography chest with and without IV contrast
Indication: Consider as an alternative to CTA. [15]
In stable patients who should avoid ionizing radiation
For serial follow-ups
Supportive findings: similar to CTA
Transthoracic echocardiography [15]
Indications
Rapid assessment in hemodynamically unstable patients
Evaluation for concomitant heart disease
Supportive findings
Dilatation of the aorta
Possible cardiac pathology
Signs of coronary artery disease [17]
Transesophageal echocardiography: allows for more accurate assessment than TTE [15]
Indication: intraoperative monitoring
Catheter angiography (aortography) [16]
Indications
Evaluation and possibly treatment of coexisting coronary artery disease
Assessment of aortic lumen and branch vessels
Supportive findings: contrast column in the lumen of the aneurysm
M: Approach
Unstable patients (e.g., in the case of rupture): emergency TAA repair (see “Thoracic aortic aneurysm rupture”)
Symptomatic patients: urgent TAA repair
Asymptomatic patients
Aneurysm surveillance
Elective TAA repair when size or growth thresholds are passed
All patients: conservative management with reduction of cardiovascular risk factors
Invasive treatment: TAA repair [13]
General indications
TAA rupture
Symptomatic TAA
Asymptomatic TAA when size or growth thresholds are passed
Indications for asymptomatic patients
The decision to perform elective TAA repair in asymptomatic patients depends on the size and expansion rate of the aneurysm. In all patients, the risks and benefits of aneurysm resection should be weighed carefully.
Open surgical repair (OSR) is recommended for patients with TAA of the ascending aorta and aneurysms involving the aortic arch. For patients with descending thoracic or thoracoabdominal aortic aneurysms, thoracic endovascular aneurysm repair (TEVAR) or OSR can be performed.
Open surgical repair (OSR) [13]
Open surgical repair is a major operation with high associated morbidity and mortality. [18]
Indications: preferred in young patients with few comorbidities and low surgical risk and patients with connective tissue disorders [18]
Symptomatic TAAs involving the ascending aorta or the aortic arch
Thoracic endovascular aneurysm repair (TEVAR) [13]
Indications: Degenerative or traumatic descending aortic aneurysms
Contraindications
Absence of a sufficiently long (2–3 cm) “landing zone” for the stent graft
Absence of adequate vascular access sites. All patients should receive conservative treatment to reduce the risk of further aneurysm expansion or rupture.
P/C: Embolism: caused by thrombotic material of the aneurysm
Aortic valve regurgitation: due to aortic root dilation
Aortic dissection
Thoracic aortic aneurysm rupture
Thoracic aortic aneurysm rupture
Risk factors
Large aneurysm diameter
Rapid aneurysm expansion
Trauma
Smoking
Clinical features
Contained rupture
Severe chest pain (may be indistinguishable from acute MI)
Possible abdominal pain in patients with thoracoabdominal aneurysms
Patients are often hemodynamically stable.
Free rupture
Possible loss of consciousness
Severe chest and possible abdominal pain
Hypotension
Acute respiratory failure
Hemoptysis
Gastrointestinal bleeding
High mortality rate
Diagnostics [13][16][15]
Initial evaluation
Hemodynamically unstable patients: no time for detailed assessment
Proceed directly to OR and consider bedside TTE.
Hemodynamically stable patients: Obtain CTA of the chest, abdomen, and pelvis with IV contrast.
Supportive findings
Extravasation of contrast
Contained rupture: perivascular hematoma sealed off by surrounding structures
Free rupture: massive hematoma
Additional diagnostic evaluation to consider (once patient has been stabilized)
ECG: to rule out STEMI as a differential diagnosis
Laboratory studies: There are no laboratory findings specific to TAA rupture.
CBC: ↓ hemoglobin, ↓ hematocrit, and ↓ red blood cell count in severe hemorrhage
ABG: metabolic acidosis in cases of shock
See “Chest pain” for workup and differential diagnoses.
Treatment
Emergency surgical repair [22]
OSR
TEVAR may be considered in patients with rupture of the descending thoracic aorta.
Complications
Bleeding into the mediastinum → cardiac tamponade (rapidly fatal)
Left hemothorax
Prognosis: Free rupture has a high mortality rate.
Cerebral aneurysm
-Types
Berry (saccular) aneurysms
Most common type of aneurysm
Associated with autosomal-dominant polycystic kidney disease, Ehlers-Danlos syndrome and Marfan syndrome, aortic coarctation, smoking, hypertension, hyperlipidemia, high alcohol consumption, familial aneurysms, estrogen deficiency
Fusiform aneurysms
Mycotic aneurysms
Traumatic aneurysms
Charcot-Bouchard microaneurysms
Associated with hypertension and diabetes.
Affect small lenticulostriate vessels in the basal ganglia and thalamus.
Their rupture is the most common cause of intracerebral hemorrhage.
-Location: The majority of cerebral aneurysms occur in the circle of Willis.
Clinical features
Usually asymptomatic
Anterior or posterior communicating artery aneurysms
Visual field defects
Oculomotor nerve palsy
In case of rupture → subarachnoid hemorrhage →Thunderclap headache: sudden onset of severely painful headache, meningism, impaired consciousness
-Diagnosis
Angiography: determines location, size, and morphology of aneurysm
See subdural hemorrhage for suspected aneurysmal subdural hemorrhage.
-Treatment
Control BP
Surgical clipping and/or endovascular coiling
Popliteal aneurysm
Most common peripheral aneurysm and second most common aneurysm after AAAs
-Epidemiology
♂ > ♀
Mean age: 65 years
Etiology: multifactorial (i.e., inflammation, immune, genetic, and mechanical factors)
-Clinical features
Usually asymptomatic mass in the popliteal fossa (50% are bilateral)
If symptomatic
Knee pain
Acute limb ischemia → 6 Ps
Chronic limb ischemia
-Diagnosis
Doppler ultrasonography (best initial): excludes Baker’s cyst; identifies thrombus and patency of vessel
CT angiography: preoperative assessment
-Complications
Rupture
Distal embolization: blue toe syndrome (small vessel occlusion caused by an embolus)
Chronic thrombosis
-Treatment
Anticoagulation (e.g., heparin)
Surgery with venous bypass graft or surgical aneurysmal excision
Indication: symptomatic or ≥ 2 cm in diameter
Ileofemoral aneurysm
Second most common peripheral aneurysm after popliteal aneurysms
-Etiology: See risk factors for atherosclerosis.
-Clinical features
May be asymptomatic
Acute limb ischemia → 6 Ps
Compression of nearby nerves or veins: sudden pain, weakness, swelling, numbness in the leg
Painless, pulsatile swelling with a palpable thrill at the mid-inguinal point
Auscultation of the swelling: loud, harsh, continuous murmur
Often associated with other aneurysms, esp. AAA and thoracic aortic aneurysm
-Diagnosis
Doppler ultrasonography (best initial test): identifies thrombus and patency of vessel
CT angiography: preoperative assessment
-Complications
Rupture: acute groin pain
Blue toe syndrome
-Treatment
Procedure: surgery with bypass or surgical excision of aneurysm
Indication
Symptomatic
IAA ≥ 3 cm
Rapidly expanding
Coexistent AAA
Complications are present
External carotid artery aneurysm
Etiology: commonly atherosclerosis, trauma (iatrogenic or penetrating injury), infection (septic emboli)
-Clinical features
Pulsatile neck mass (below angle of mandible)
Associated bruit
Transient ischemic attacks (TIAs) or stroke
Mass effect on adjacent structures (veins and nerves → hoarseness, facial swelling, difficulty swallowing)
-Diagnosis
Ultrasound (initial): evidence of swirling blood with a thrombus
CT or MR angiography: determines the site and size of the aneurysm, excludes rupture or other pathologies
-Complications
Rupture: airway compression, pharyngeal hemorrhage, epistaxis
Neck infection: pain, fever
-Treatment: surgical repair, either in the form of an aneurysm excision and reconstruction or endovascular repair (grafting or stenting
Ventricular aneurysm
-Etiology
Myocardial infarction (occurs in 8–15% of patients; 2 weeks to months after MI)
Risk factors
Complete occlusion of the left anterior descending coronary artery
Absent angina
-Location: ∼ 85% in the anterior or apical walls, 10–15% in the inferior-basal walls of the left ventricle
-Clinical features
Enlarged heart on percussion
Diffuse and displaced apical pulse to left midclavicular line
3rd and 4thheart sounds
Systolic murmur (mitral regurgitation)
-Diagnosis
ECG: persistent ST elevation
Echocardiography (or CT or MRI ): dyskinetic wall motion and diastolic deformity
-Complications
Arrhythmias
Ventricular rupture → cardiac tamponade
Thrombus formation → thromboembolism (stroke, mesenteric ischemia, renal infarction)
Heart failure
-Treatment
Small and asymptomatic: conservative treatment with regular follow-up
If large, symptomatic, or there is evidence of a thrombus
ACE inhibitors
Anticoagulation
If not responsive to medical therapy: surgical resection of the aneurysm
Types of aneurysms
True aneurysms are an abnormal dilation of an artery due to a weakened vessel wall. By contrast, false aneurysms are external hematomas with a persistent communication to a leaking artery. Dissections are a separation of the arterial wall layers caused by blood entering the intima-media space after a tear in the internal layer occurred. Aneurysms are differentiated according to their location. This card discusses the etiology and clinical features of cerebral, external carotid, Ileofemoral, popliteal, and ventricular aneurysms. Symptoms generally depend on the location and size of the aneurysm. There are surgical and endovascular treatment options, the choice of which depends on the specific type of aneurysm and if symptoms or complications are present.
For more specific information on individual types of aneurysms, see the articles on thoracic aortic aneurysm, abdominal aortic aneurysm, aortic dissection, dissection of the carotid and the vertebral artery, and subarachnoid hemorrhage.
Acute limb ischemiaa
D: acute arterial occlusion of an extremity. Acute limb ischemia (ALI) is a vascular emergency in which the arterial blood supply to one or more extremities is critically reduced. Arterial thrombosis and cardiac emboli are responsible for the majority of cases.
Acute limb ischaemia is defined as the sudden decrease in limb perfusion that threatens the viability of the limb.
Complete or even partial occlusion of the arterial supply to a limb can lead to rapid ischaemia and poor functional outcomes within hours.
In this article, we shall look at the causes, clinical features and management of a patient with acute limb ischaemia.
R:
D: The differential diagnoses for acute limb ischaemia include critical chronic limb ischaemia, acute DVT (can present as Phlegmasia cerulea dolens and Phlegmasia alba dolens), or spinal cord or peripheral nerve compression. These are subtypes: Leriche syndrome (aortoiliac occlusive disease) –> occlusion at the level of the aortic bifurcation or bilateral occlusion of the iliac arteries that usually presents with: pain in both legs and the buttocks, bilaterally absent femoral, popliteal and ankle pulses, erectile dysfunction, shock. Hair tourniquet syndrome: a condition in which a hair or thread becomes wound around an appendage tightly, putting the appendage at risk of ischemic damage.
E:
A: Acute limb ischaemia has an incidence of around 1.5 per 10,000 person years. Its causes can be classified into 3 main groups:
Embolisation whereby a thrombus from a proximal source travels distally to occlude the artery (most common)
The original thrombus source may be as a result of AF, post-MI mural-thrombus, abdominal aortic aneurysm, or prosthetic heart valves
Thrombosis in situ whereby an atheroma plaque in the artery ruptures and a thrombus forms on the plaque’s cap (presenting as acute or acute-on-chronic)
Trauma (less common), including compartment syndrom
Arterial occlusion
-Thrombosis
–Peripheral arterial disease
–Stent or graft thrombosis
–Aneurysmal thrombosis (most commonly popliteal aneurysms)
–Vasculitis, thrombophilia (rare)
-Embolism
–Cardiac emboli
—>Atrial fibrillation (most common)
—>Myocardial infarction
–Cholesterol embolism (e.g., blue toe syndrome)
–DVT (paradoxical embolism via a patent foramen ovale)
–Septic emboli (e.g., from endocarditis)
–Proximal aneurysms (aortic, popliteal) or atherosclerotic lesions
-Trauma leading to transsection, dissection, or thrombosis of a vessel
–Posterior knee dislocations (e.g., popliteal artery thrombosis)
–Iatrogenic injury at the site of arterial access (e.g., femoral artery thrombosis)
–Crush injury of a limb
-Aortic dissection
-Compartment syndrome
-Venous occlusion (phlegmasia cerulea dolens)
C:
Classically, the signs and symptoms of acute limb ischaemia can be described using the 6 Ps (the first three here being the most common initial features):
Acute limb ischaemia is often characterised by a sudden onset of these symptoms. A normal, pulsatile contralateral limb is a sensitive sign of an embolic occlusion.
In the history, the causes of potential embolisation should be explored. These include chronic limb ischaemia, atrial fibrillation, recent MI (resulting in a mural thrombus), or a symptomatic AAA (ask about back/abdominal pain) and peripheral aneurysms.
The later the patient presents to a hospital, the more likely that irreversible damage to the neuromuscular structures will have occurred (more common >6hrs post-symptom onset), which will ultimately result in a paralysed limb.
Pain
Pallor
Pulselessness
Paresthesia
Perishingly cold
Paralysis
The lower limb is affected in > 80% of cases.
Arterial thrombosis: subacute onset; history of claudication pain
Embolism: acute onset; history of heart disease (e.g., atrial fibrillation)
The 6 Ps distal to the site of occlusion
Pain
Pallor
Pulselessness
Paralysis
Paresthesia
Poikilothermia
P:
I:
Routine bloods, including a serum lactate (to assess the level of ischaemia), a thrombophilia screen (if <50yrs without known risk factors), and a group and save, should be taken, along with an ECG.
Suspected cases should be initially investigated with beside Doppler ultrasound scan (both limbs), followed by considering a CT angiography (Fig. 2).
If the limb is considered to be salvageable, a CT arteriogram can provide more information regarding the anatomical location of the occlusion and can help decide the operative approach (such as femoral vs. popliteal incision).
Tests to confirm the diagnosis and identify the site(s) of occlusion
Best initial test: arterial and venous Doppler
Diminished or absent Doppler flow signal distal to site of occlusion.
Confirmatory test: angiography (DSA, CTA, MRA)
Digital subtraction angiography (DSA) is the imaging modality of choice.
Should only be performed if delaying treatment for further imaging does not threaten the extremity
Depending on the suspected etiology, other tests may be indicated (e.g., echocardiography if an arterial embolism is suspected).
M:
Initial Management
Acute limb ischaemia is a surgical emergency. Complete arterial occlusion will lead to irreversible tissue damage within 6 hours. Early senior surgical support is vital.
Start the patient on high-flow oxygen and ensure adequate IV access. A therapeutic dose heparin or preferably a bolus dose then heparin infusion should be initiated as soon as is practical.
Conservative Management
Conservative management can often be considered those Rutherford 1 and 2a; a prolonged course of heparin may be the most effective non-operative management of acute limb ischaemia.
Any patient started on conservative management via heparin will need regular assessment to determine its effectiveness through monitoring APPT and clinical review. Surgical interventions may be warranted if no significant improvement is seen.
Surgical Intervention
Surgical intervention is mandatory for cases presenting in Rutherford 2b
If the cause is embolic, the options are:
Embolectomy via a Fogarty catheter
Local intra-arterial thrombolysis*
Bypass surgery (if there is insufficient flow back)
If the cause is due to thrombotic disease, the options are:
Local intra-arterial thrombolysis
Angioplasty (Fig. 3)
Bypass surgery.
Irreversible limb ischaemia (mottled non-blanching appearance with hard woody muscles) requires urgent amputation or taking a palliative approach.
Most post-operative cases require a high level of care, typically at a high dependency unit, due to the ischaemia reperfusion syndrome.
*Intra-arterial thrombolysis is often difficult to conduct within 6 hours, therefore often used for Rutherford 2a
Long Term Management
Reduction of the cardiovascular mortality risk in this patient group is key. Promoting regular exercise, smoking cessation, and weight loss as necessary.
Most cases should be started on an anti-platelet agent, such as low-dose aspirin or clopidogrel, or even anticoagulation with warfarin or a DOAC. Any underlying predisposing conditions to the acute limb ischaemia should be treated, e.g. uncontrolled AF.
Cases resulting in amputation will require occupational therapy and physiotherapy, with a long term rehabilitation plan discussed and transfer to an intermediate rehabilitation centre.
Systemic anticoagulation with an IV heparin bolus followed by continuous infusion unless a contraindication is present
Further management depends on the severity of acute limb ischemia.
Viable, non-threatened limb
Urgent angiography to localize the site of the occlusion
Revascularization procedure (open or catheter-directed thrombectomy or thrombolysis) within 6–24 hours
Threatened limb: emergent revascularization procedure within 6 hours
First-line: catheter-directed thrombolysis and/or percutaneous mechanical thromboembolectomy (e.g., balloon catheter embolectomy)
Second-line: open thromboembolectomy
Non-viable limb: limb amputation
Acute limb ischemia due to compartment syndrome: fasciotomy (see compartment syndrome)
Acute limb ischemia due to a dissecting aneurysm: stenting and/or surgical repair
P: Permanent nerve damage: sensory loss, muscle weakness, paralysis
Loss of limb due to irreversible ischemia
Reperfusion injury (postischemic syndrome)
Following reperfusion, detached metabolites may trigger further complications, especially after prolonged occlusion (more than 6 h).
Possible complications
Acidosis, hyperkalemia → cardiac arrhythmia
Rhabdomyolysis → myoglobinemia → crush syndrome
Ischemia-reperfusion injury → compartment syndrome
Massive edema → hypovolemic shock
Severe complications: DIC (disseminated intravascular coagulation), multiorgan dysfunction
Symptomatic treatment, monitoring (amputation of the affected extremity if necessary).
Complications: Acute limb ischaemia has a mortality rate of around 20%, with the 30-day mortality rate following the surgical treatment of acute limb ischaemia at 15%.
An important complication of acute limb ischaemia is reperfusion injury; sudden increase in capillary permeability can result in:
Compartment syndrome
Release of substances from the damaged muscle cells, such as:
K+ ions causing hyperkalaemia
H+ ions causing acidosis
Myoglobin, resulting in significant AKI
It is imperative that patients at risk of compartment syndrome are closely monitored and rapidly treated. Electrolyte imbalance due to reperfusion injury requires close monitoring and potentially haemofiltration.
Chronic limb ischaemia
D: Chronic limb ischaemia is peripheral arterial disease that results in a symptomatic reduced blood supply to the limbs.
It is typically caused by atherosclerosis (rarely vasculitis) and will commonly affect the lower limbs (however the upper limbs and gluteals can also be affected).
R: Smoking Diabetes mellitus Hypertension Hyperlipidaemia Increasing age Family history Obesity and physical inactivity
D: There are two major differential diagnoses* for a patient presenting with limb ischaemia symptoms:
Spinal stenosis (‘neurogenic claudication’)
Typically have pain from the back radiating down the lateral aspect of the leg (tensor fascia lata), often have symptoms on initial movement or symptoms that are relieved by sitting rather than standing
Acute limb ischaemia
Clinical features that are less than 14 days duration, often presenting within hours.
*Acute-on-chronic ischaemia is a more complex condition whereby there is an acute often embolic event in a patient with previous peripheral arterial disease. These patients are sub-classified as they typically have a longer duration in which the limb is salvageable.
E: Around 15-20% individuals over 70yrs have peripheral arterial disease. The Framingham study demonstrated an increase in the prevalence of the disease from 0.4 per 1000 males aged 35-45yrs to 6 per 1000 males aged >65yrs.
A:
C: The clinical features of chronic limb ischaemia depend on its severity, as shown in Table 1.
One of the earlier symptoms is intermittent claudication, a cramping-type pain in the calf, thigh, or buttock after walking a fixed distance (the ‘claudication distance’), relieved by rest within minutes.
Stage 1: asymptomatic.
Stage 2: Intermittent claudication
Stage 3: Ischaemic rest pain.
Stage 4: Ulceration or gangrene, or both.
P:
I:
The ankle-brachial pressure index (ABPI, Fig. 2) is used to confirm the diagnosis and quantify severity of chronic limb ischaemia: Normal = >0.9, mild (0.8-0.9), moderate (0.5-0.8), severe (<0.5). Any ABPI value >1.2 should be interpreted with caution, as calcification and hardening of the arteries may cause a falsely high ABPI.
Buerger’s test involves lying the patient supine and raising their legs until they go pale and then lowering them until the colour returns (or even becoming hyperaemic). The angle at which limb goes pale is termed Buerger’s angle; an angle of less than 20 degrees indicates severe ischaemia.
Any critical limb ischaemia should be investigated initially with a Doppler ultrasound, used to assess the severity and anatomical location of any occlusion. Further imaging can be achieved via CT angiography or MR angiography (MRA).
Due to concurrent cardiovascular risk factors seen in patients with chronic limb ischaemia, patients should also have a cardiovascular risk assessment. This includes blood pressure, blood glucose, lipid profile and ECG.
In addition, any patient presenting with chronic limb ischaemia <50yrs without significant risk factors should also have a thrombophilia screen and homocysteine levels* checked.
*A lower homocysteine level has been associated with reduced risk of cardiovascular events
M:Medical Management
Most patients with chronic limb ischaemia require cardiovascular risk factor modification:
Lifestyle advice (smoking cessation, regular exercise, weight reduction) Statin therapy (ideally atorvastatin 80mg OD) Anti-platelet therapy (ideally clopidogrel 75mg OD) Optimise diabetes control Enrollment into a local supervised exercise programme has been shown to improve walking distance and claudication distance, and should be used as first line therapy in any patient without critical limb ischaemia
The course of chronic limb ischaemia is variable and many patients’ symptoms do improve on lifestyle changes and medical management alone.
Surgical Management
NICE guidance states that surgical intervention can be offered in suitable patients if (i) risk factor modification has been discussed; and (ii) supervised exercise has failed to improve symptoms.
Any patients with critical limb ischaemia should be urgently referred for surgical intervention.
There are two main surgical options available:
Angioplasty with or without stenting (Fig. 3)
Bypass grafting, typically used for diffuse disease or in younger patients
A combination such as surgery to clean a specific lesion allowing access for angioplasty to another region
Amputations are considered for any patients who are unsuitable for revascularisation with ischaemia causing incurable symptoms or gangrene leading to sepsis.
P: Critical limb ischaemia is the advanced form of chronic limb ischaemia.
It can be clinically defined in three ways:
Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia
Presence of ischaemic lesions or gangrene objectively attributable to the arterial occlusive disease (Fig. 1)
ABPI less than 0.5
On examination, the limbs may be pale and cold, with weak or absent pulses. Other signs include limb hair loss, skin changes (atrophic skin, ulceration, or gangrene), and thickened nails.
Chronic limb ischaemia can result in sepsis (secondary to infected gangrene), acute-on-chronic ischaemia, amputation*, and reduced mobility and quality of life.
*Amputation is eventually required in 1-2% (increases to 5% in people with diabetes)
Over a 5 year period, of those patients with intermittent claudication:
Most will have stable claudication
10-20% develop worsening symptoms
5-10% develop critical limb ischaemia
Two years following a below-knee amputation for chronic limb ischaemia, 15% require a further above knee amputation, 30% have died, and only 40% have full mobility.
The 5 year mortality rate in those diagnosed with chronic limb ischaemia is around 50%.
Circulatory failure/Shock
Shock means that organs are hypoperfused and that means they will begin to fail without aggressive intervention. It is likely that hypovolaemia and sepsis will be responsible for the majority of the shock you deal with as an inpatient, but do remember that other types of shock are possible (the management for sepsis, hypovolaemia, and anaphylaxis can be found elsewhere on the site)
If the patient is deteriorating, ensure early access and insert a wide bore cannula (ideally a grey or orange) in each antecubital to allow the most prompt fluid resuscitation.
Start IV fluid replacement in an attempt to increase the intravascular volume, to increase the blood pressure and the perfusion of the organs but the constituents of the fluid are important.
Try to give the same fluid that you are losing such as blood in haemorrhage and keep the electrolytes balanced (these can become depleted in nausea and diarrhoea in particular). A good start is using crystalloids in rapid 250ml bolus, reassessing after each bag.*
*Be careful not to run through bags with added potassium chloride ‘stat’, as rapid boluses of potassium can cause cardiac arrest.
Autotransfusion
Raising the patient’s legs can be a good initial step while fluids are being made up as it delivers an ‘autotransfusion’ (uses gravity to redistribute the patient’s own blood more centrally to increase the blood pressure.)
Any sick patient should have concurrent blood samples taken for full blood count, urea and electrolytes, coagulation, liver biomarkers, troponins, venous gas samples for lactate and cultures as required and they should also undergo a 12 lead ECG to explore whether the shock is of cardiac origin
If you suspect post-operative complications, including internal haemorrhage which would not be amenable to simple compression, then you need to notify your team urgently for further assessment and potentially returning to theatre to explore and manage. Blood (rather than just serosanguinous fluid) in drains, disproportionate pain, and signs of peritonism can all be clues to support any suspected pathology.
Ruptured AAA
75% die before reaching hospital.
Retroperitoneal vs free rupture.
When you have got a big aneurysm, the peritoneum becomes stretched over the front of it. So if a rupture occurs, it can occur into the retroperitoneal space, where there is less space, so blood will accumulate, can tamponade the rupture. These are the people most likely to make it to hospital.
Or you can have a rupture in the anterior part, which will rupture through the peritoneum, and then you’ve got this huge great cavity, so the chances of tamponade are lower, these are the people at risk, need to get them to theatre.
Describe permissive hypotension in AAA
Permissive hypotension: a concept used in trauma and resuscitation situation where you allow a lower BP than you would do otherwise. So if you’ve got someone with a ruptured aneurysm, you want to make sure they are perfusing their brain, etc. before you get them to theatre, but you don’t want to give them so much fluid that you drive their bp up, and blow off any clot that is formed or tamponading their aorta at the time.
Patients with ruptured AAA need to have CT before theatre as that can help with decision of open surgery or EVAR.
Post operative complications: cardiovascular (MI), respiratory (LRTI, ARDS), CNS (stroke), GI (abdominal compartment syndrome, ischaemic gut), renal (AKI), bleeding, distal limb ischaemia, wound infection.
Surgery for AAA
Surgery threshold for aneurysm: >5.5cm. Need to have done a CT scan to help with decision of open surgery or EVAR.
-Where the aneurysm is, will show complexity of the surgery.
EVAR is preferable for physiologically deranged patients. In this we need to get in through common femoral arteries and get quite a big device, up through the iliac system into the aorta. So we need to know if their access vessels are big enough. You want to exclude that aneurysm sac from the circulation. So you will either sew in a tube, or you will put in a stent, both of which will carry blood through aneurysm sac, so it is completely excluded.
Open repair
Midline laparotomy
Duodenum and small bowel out of the way.
Dissect the duodenum off the aorta.
Clamps above aneurysm and below –> may be on aorta or iliac vessels.
Open up aneurysm.
Stitch in graft.
It is a huge operation:
-clamping the aorta.
–>end organ ischaemia –> kidney, gut, spine, legs, causes huge haemodynamic changes.
Increased SVR (increased preload and afterload)
-Reperfusion injury (mediated by inflammatory cytokines).
Massive blood loss
Transfusion related coagulopathy.
Post operative complications: cardiovascular (MI), respiratory (LRTI, ARDS), CNS (stroke), GI (abdominal compartment syndrome, ischaemic gut), renal (AKI), Bleeding, distal limb ischaemia, wound infection.
Late operations: graft infection/anastomotic pseudoaneurysm, aorto-enteric fistula, small bowel obstruction, incisional hernia.
EVAR: Endovascular aneurysm repair
Avoids laparotomy
Acoids aortic clamping-no hypovolemic shift, ischemic, re-perfusion problems.
Everything is done through groin: per cutaneously –> only small incision needed, doesn’t require stitches.
The device is inserted up on iliac system, under x-ray guidance is positioned and deployed, then open (blown up).
EVAR complications:
- generally less significant with open repair.
- wide trauma/access problems.
- Endoleak: to patients requiring life-long surveillance. Blood tracking back into the aneurysmal sac, in between the vessel wall eg. graft.
This can happen because there is inadequate seal at the top or bottom ends, or retrograde flow from lumbars or branches.
Or tears in fabric of graft, leaks in between different components. Therefore all patients who have an EVAR will need life long surveillance with ultrasound.
What is a cross clamped Aorta?
An aortic cross-clamp is a surgical instrument used in cardiac surgery to clamp the aorta and separate the systemic circulation from the outflow of the heart.
An aortic cross-clamping procedure serves, for example, in the repairing of coarctation of the aorta. In newborns, the treatment of choice for this condition is resection and primary anastomosis. The clamping of the aorta excludes the systemic circulation, by definition, thus causing an ischemia. When a long cross-clamping period (longer than 25 min) or a drop in distal aortic pressure below 50–60 mmHg is anticipated, the use of an intraoperative shunt may prevent complications such as paraplegia.
In the surgical treatment of abdominal aortic aneurysm, the single proximal cross-clamp can be placed at 3 alternative aortic levels: infrarenal, hiatal, and thoracic.
Performed in open repair surgery of abdominal aortic aneurysms.
The clinical status of the patient and the degree of operative urgency–as determined by the extent of the aneurysm–generally dictate the proximal clamp location.
Patients who present with aneurysmal rupture or hypovolemic shock benefit from thoracic clamping, because it restores the blood pressure and allows time to replace the volume deficit. Infrarenal placement is advantageous in patients with intact aneurysms if there is sufficient space for the clamp between the renal arteries and the aortic aneurysm. In patients with juxtarenal aneurysms, hiatal clamping enables safe and easy anastomosis to the healthy aorta. Clamping at this level also helps prevent late anastomotic aneurysm formation, which is frequently encountered after inadvertent anastomosis of the graft to a diseased portion of the aorta.
However, clamping the aorta causes end organ ischaemia and causes huge haemodynamic changes. It will also cause increased SVR (increased pre-load and afterload). It also causes reperfusion injury (mediated by inflammatory cytokines). N
Acute coronary syndrome
D: Myocardial infarction: myocardial cell death caused by prolonged ischemia [1][2]
Acute coronary syndrome: suspicion or confirmed presence of acute myocardial ischemia and/or myocardial infarction
Further classified as unstable angina, NSTEMI, and STEMI
Sudden cardiac death (SCD): sudden, unexpected death caused by loss of cardiac function (most commonly due to lethal arrhythmia, e.g., ventricular fibrillation).
Unstable Angina
ST Elevation Myocardial Infarction (STEMI)
Non-ST Elevation Myocardial Infarction (NSTEMI)
Acute Coronary Syndrome is an umbrella term for a spectrum of disease caused by ischaemia (and in some cases infarction) of myocardium (loss of blood supply to heart muscle). It is a medical emergency and required immediate hospital admission.
STEMI – ST elevation MI
Diagnosable on the basis of classical ECG changes
NSTEMI – non-ST elevation MI
Usually diagnosed on the basis of a suggestive history, with positive biochemical markers – e.g. positive troponin
Unstable angina – ischaemia, without infarction
No obviously evident ECG changes (there may be some transient changes), negative troponin, often a history suggestive of ACS. Unstable angina is significant due to the high risk (50%) of MI in the subsequent 30 days. Not to be confused with stable angina
They are grouped together because – they all have a common mechanism – rupture or erosion of the fibrous cap of a coronary artery plaque
R: Risk factors: See atherosclerosis. Increasing age Male gender Personal history of angina and/or known coronary artery disease Family history of CAD Diabetes mellitus Systolic hypertension Tobacco use Hyperlipidemia
D: if person rests and pain goes away: stable angina (no cardiac enzymes in blood). Differential diagnosis of increased troponin Cardiac causes Myocarditis Decompensated congestive heart failure Pulmonary embolism Cardiac arrhythmia, tachycardia Cardiac trauma Takotsubo cardiomyopathy Noncardiac causes Renal failure Stroke Critical illness (e.g., sepsis) Differential diagnosis of ST-elevations on ECG [11] Early repolarization LBBB Brugada syndrome Myocarditis Pericarditis Pulmonary embolism Hyperkalemia Tricyclic antidepressant use Poor ECG lead placement.
E: Incidence
∼ 1.5 million cases of myocardial infarction per year in the US
♂ > ♀ (3:1).
A:
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”.
Most common cause: coronary artery atherosclerosis
Less common
Coronary artery dissection
Coronary artery vasospasm (e.g., Prinzmetal angina, cocaine use)
Takotsubo cardiomyopathy
Myocarditis
Thrombophilia (e.g., polycythemia vera)
Coronary artery embolism (e.g., due to prosthetic heart valve, atrial fibrillation)
Vasculitis (e.g., polyarteritis nodosa, Kawasaki syndrome)
Myocardial oxygen supply-demand mismatch
Hypotension
Severe anemia
Hypertrophic cardiomyopathy
Severe aortic stenosis.
C: Classic presentation Acute retrosternal chest pain Typically described as dull, squeezing pressure and/or tightness Commonly radiates to left chest, arm, shoulder, neck, jaw, and/or epigastrium Precipitated by exertion or stress See also angina. The peak time of occurrence is usually in the morning (8–11 a.m.). Dyspnea (especially with exertion) Pallor Nausea, vomiting Diaphoresis, anxiety Dizziness, lightheadedness, syncope
Other findings
Tachycardia, arrhythmias
Symptoms of CHF (e.g., orthopnea, pulmonary edema) or cardiogenic shock (e.g., hypotension, tachycardia, cold extremities)
New heart murmur on auscultation (e.g., new S4)
More common in inferior wall infarction
Epigastric pain
Bradycardia
Clinical triad in right ventricular infarction: Hypotension, elevated jugular venous pressure, clear lung fields.
Atypical presentation: minimal to no chest pain
More likely in elderly, diabetic individuals, and women
Autonomic symptoms (e.g., nausea, diaphoresis) are often the chief complaint.
In patients with diabetes, chest pain may be completely absent (e.g., silent MI) due to polyneuropathy.
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”.
P: ACS is most commonly due to unstable plaque formation and subsequent rupture.
Plaque formation and rupture
For plaque formation, see coronary artery disease and atherosclerosis.
Stable atherosclerotic plaque: manifests as stable angina (symptomatic during exertion)
Unstable plaques are lipid-rich and covered by thin fibrous caps → high risk of rupture
Inflammatory cells in the plaque (e.g., macrophages) secrete matrix metalloproteinases → breakdown of extracellular matrix → weakening of the fibrous cap → minor stress → rupture of the fibrous cap → exposure of highly thrombogenic lipid core → thrombus formation → coronary artery occlusion.
Coronary artery occlusion
Partial coronary artery occlusion
Decreased myocardial blood flow → supply-demand mismatch → myocardial ischemia
Usually affects the inner layer of the myocardium (subendocardial infarction)
Typically manifests clinically as unstable angina and/or NSTEMI
Complete coronary artery occlusion
Impaired myocardial blood flow → sudden death of myocardial cells (if no reperfusion occurs)
Usually affects the full thickness of the myocardium (transmural infarction)
Typically manifests clinically as STEMI.
I:
When a patient presents with possible ACS symptoms (i.e. chest pain) perform an ECG:
If there is ST elevation or new left bundle branch block the diagnosis is STEMI.
If there is no ST elevation then perform troponin blood tests:
If there are 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 musculoskeletal chest pain.
ECG Changes in Acute Coronary Syndrome
STEMI:
ST segment elevation in leads consistent with an area of ischaemia
New Left Bundle Branch Block also diagnoses a “STEMI”
NSTEMI:
ST segment depression in a region
Deep T Wave Inversion
Pathological Q Waves (suggesting a deep infarct – a late sign).
ECG should be performed immediately once ACS is suspected, followed by measurement of cardiac biomarkers. Further diagnostic workup (e.g., echocardiography) depends on the results of initial evaluation and further risk stratification (e.g., TIMI score).
ECG
12-lead ECG is the best initial test if ACS is suspected.
Dynamic changes require serial ECG evaluation.
Compare to prior ECGs (if available).
ECG changes in STEMI [17]
Acute stage: myocardial damage ongoing
Hyperacute T waves (“peaked T wave”)
ST elevations in two contiguous leads with reciprocal ST depressions
Intermediate stage: myocardial necrosis present
Absence of R wave
T-wave inversions
Pathological Q waves
Chronic stage: permanent scarring
Persistent, broad, and deep Q waves
Often incomplete recovery of R waves
Permanent T wave inversion is possible.
ECG changes in NSTEMI/unstable angina
No ST elevations present
Nonspecific changes may be present.
ST depression
Inverted T wave
Loss of R wave.
Troponins are proteins found in cardiac muscle. The specific type of troponin, the normal range and diagnostic criteria vary based on different laboratories (so check your policy). Diagnosis of ACS typically requires serial troponins (e.g. at baseline and 6 or 12 hours after onset of symptoms). A rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle. They are non-specific, meaning that a raised troponin does not automatically mean ACS.
There are alternative causes of raised troponins:
Chronic renal failure Sepsis Myocarditis Aortic dissection Pulmonary embolism Perform all the investigations you would normally arrange for stable angina:
Physical Examination (heart sounds, signs of heart failure, BMI) ECG FBC (check for anaemia) U&Es (prior to ACEi and other meds) LFTs (prior to statins) Lipid profile Thyroid function tests (check for hypo / hyper thyroid) HbA1C and fasting glucose (for diabetes) Plus:
Chest xray to investigate for other causes of chest pain and pulmonary oedema
Echocardiogram after the event to assess the functional damage
CT coronary angiogram to assess for coronary artery disease.
Additional findings [22][23]
Elevated inflammatory markers: ↑ WBC, CRP
Elevated BNP: especially in heart failure
Elevated LDH
Elevated AST (SGOT)
Coronary angiography
Best test for definitive diagnosis of acute coronary occlusion
Can be used for concurrent intervention (e.g., PCI with stent placement)
Can identify site and degree of vessel occlusion
Indications include
Acute STEMI
Other high-risk ACS (see TIMI score below)
See also cardiac catheterization.
Transthoracic echocardiogram
Identification of any wall motion abnormalities and to assess LV function
Important for risk assessment: In STEMI, the best predictor of survival is LVEF.
Evaluation for complications: aneurysms, mitral valve regurgitation, pericardial effusion, free wall rupture
Cardiac CT
May be considered as an alternative to invasive coronary angiography in patients with an intermediate risk of ACS (based on TIMI score)
Allows for noninvasive visualization of the coronary arteries
Contraindication: arrhythmias, tachycardia.
M: All patients [11][5]
Monitoring
Serial 12-lead ECG
Continuous cardiac monitoring
Serial serum troponin measurement
Pharmacologic therapy
Sublingual or intravenous nitrate (nitroglycerin or ISDN)
For symptomatic relief of chest pain
Does not improve prognosis
Contraindications: inferior wall infarct (due to risk for hypotension), hypotension, and/or PDE 5 inhibitor (e.g., sildenafil) taken within last 24 hours
Morphine IV or SC (3–5 mg)
Only if the patient has severe, persistent chest pain or severe anxiety related to the myocardial event
Administer with caution due to increased risk of complications (e.g., hypotension, respiratory depression) and adverse events
Beta blocker
Recommended within the first 24 hours of admission
Avoid in patients with hypotension, features of heart failure, and/or risk of cardiogenic shock (e.g., large LV infarct, low ejection fraction).
Statins: early initiation of high-intensity statin (such as atorvastatin 80 mg) regardless of baseline cholesterol, LDL, and HDL levels
Loop diuretic (e.g., furosemide) if the patient has flash pulmonary edema or features of heart failure
Supportive care
Intravenous fluids (e.g., normal saline): in patients with an inferior MI that causes RV dysfunction
Oxygen: only in case of cyanosis, severe dyspnea, or SpO2 < 90% (< 95% in STEMI).
Immediate revascularization
Revascularization is the most important step in the management of acute STEMI and initiation of further therapies (e.g., DAPT, anticoagulation) should not delay this step in management.
Emergent coronary angiography: with percutaneous coronary intervention (PCI)
Preferred method of revascularization
Balloon dilatation with stent implantation (see cardiac catheterization)
Ideally, door-to-PCI time should be < 90 minutes. It should not exceed 120 minutes.
Thrombolytic therapy: tPA, reteplase, or streptokinase
Indications:
If PCI cannot be performed < 120 minutes after onset of STEMI
If PCI was unsuccessful
No contraindications to thrombolysis
Contraindications
Any prior intracranial bleeding
Recent large GI bleeding
Recent major trauma, head injury, and/or surgery
Ischemic stroke within the past 3 months
Hypertension (> 180/110 mm Hg)
Known coagulopathy
Timing
Symptom onset was within the past 3–12 hours
Should be administered within < 30 minutes of patient arrival to the hospital
Contraindicated if > 24 hours after symptom onset
PCI should be performed even if lysis is successful.
Coronary artery bypass grafting
Not routinely recommended for acute STEMI
Indications
If PCI is unsuccessful
If coronary anatomy is not amenable to PCI
If STEMI occurs at the time of surgical repair of a mechanical defect
Medical therapy
Dual antiplatelet therapy: start as soon as possible
Aspirin loading dose 162 mg–325 mg
PLUS ADP receptor inhibitor: prasugrel, ticagrelor, or clopidogrel
Dual antiplatelet therapy should be continued for at least 12 months after PCI with DES.
GP IIb/IIIa receptor antagonist (e.g., eptifibatide or tirofiban): should be considered in precatheterization setting
Anticoagulation
Heparin or bivalirudin recommended
Continue until PCI is performed or for 48 hours after a fibrinolytic is given.
Unstable angina/NSTEMI [5]
Dual antiplatelet therapy: start as soon as possible
Aspirin loading dose
Plus ADP receptor inhibitor: clopidogrel or ticagrelor
Dual antiplatelet therapy should be continued for at least 12 months if PCI with DES was performed.
Anticoagulation
Heparin or enoxaparin
Continue for the duration of hospitalization or until PCI is performed.
Immediate vs. delayed revascularization
The indication for and timing of revascularization depends on the mortality risk (e.g., TIMI score).
In patients with therapy-resistant chest pain, a TIMI score ≥ 3, ↑ troponin, and/or ST changes > 1 mm
Consider the addition of a GPIIb/ IIIa inhibitor (e.g., tirofiban or eptifibatide)
Plan for revascularization within 72 hours (e.g., angiography with PCI or CABG).
P: TIMI score for unstable angina/NSTEMI [30]
Method for calculating the risk of mortality in patients with unstable angina or NSTEMI
Can be used to determine recommended therapeutic regimen and timing for revascularization
Interpretation
An increasing score is associated with a higher risk of mortality, new or recurrent myocardial infarction, and need for urgent revascularization (e.g., progression of unstable angina to STEMI)
Risk score ≥ 3
Early angiography recommended
Consider addition of glycoprotein IIb/IIIa inhibitor and treatment with enoxaparin (rather than UFH).
0–24 hours post-infarction
Sudden cardiac death (SCD)
Definition: A sudden death presumably caused by cardiac arrhythmia or hemodynamic catastrophe, which occurs either within an hour of symptom onset in patients with cardiovascular symptoms, or within 24 hours of being asymptomatic in patients with no cardiovascular symptoms.[37]
Pathophysiology: Fatal ventricular arrhythmia is considered to be the underlying mechanism of SCD. [38]
Underlying conditions
Coronary artery disease: present in ∼ 70% of cases in adults over 35 years [39]
Dilated/hypertrophic cardiomyopathy
Hereditary ion channelopathies (e.g., long QT syndrome, Brugada syndrome)
Prevention: installation of the implantable cardioverter-defibrillator device [38]
Arrhythmias (a common cause of death in MI patients in the first 24 hours)
Ventricular tachyarrhythmias
AV block
Asystole
Atrial fibrillation
Acute left heart failure: death of affected myocardium → absence of myocardial contraction → pulmonary edema
Cardiogenic shock
1–3 days post-infarction
Early infarct-associated pericarditis
Typically occurs within the first week of a large infarct close to the pericardium
Clinical features of acute pericarditis: pleuritic chest pain , dry cough , friction rub, diffuse ST elevations on ECG
Treatment: supportive care
Complications (rare): hemopericardium, pericardial tamponade
3–14 days post-infarction
Papillary muscle rupture
Usually occurs 2–7 days after myocardial infarction
Can lead to acute mitral regurgitation
Rupture of the posteromedial papillary muscle due to occlusion of the posterior descending artery is most common.
Clinical features
New holosystolic, blowing murmur over the 5th ICS on the midclavicular line
Signs of acute mitral regurgitation: dyspnea, cough, bilateral crackles, hypotension
Ventricular septal rupture
Usually occurs 3–5 days after myocardial infarction
Pathophysiology: macrophagic degradation of the septum → ventricular septal defect → blood flow from LV to RV following the pressure gradient (left-to-right shunt) → increased pressure in RV and increased O2 content in the venous blood
Most commonly due to LAD infarction (septal arteries arise from LAD)
Clinical features
New holosystolic murmur over the left sternal border
Acute-onset right heart failure (jugular venous distention, peripheral edema)
Can progress to cardiogenic shock: tachycardia, hypotension, cool extremities, altered mental status
Treatment: emergency surgery and revascularization (often via CABG)
Left ventricular free wall rupture
Usually occurs 5–14 days after myocardial infarction
Greatest risk during macrophage-mediated removal of necrotic tissue
LV hypertrophy and tissue fibrosis from previous MI decrease the risk of free wall rupture.
Clinical features: chest pain, dyspnea, signs of cardiac tamponade (e.g., Beck triad)
Complications: cardiac tamponade , sudden cardiac death (if the rupture occurs acutely)
Left ventricular pseudoaneurysm
Usually occurs 3–14 days after myocardial infarction
Refers to the outpouching of the ventricular wall rupture that is contained by either the pericardium, a thrombus, or scar tissue
Associated with mural thromboembolism, decreased cardiac output, and increased risk of arrhythmia
Posterolateral myocardial infarction with impending wall rupturePericardial tamponade: opened pericardium (2/2)Ruptured papillary musclePapillary muscle rupture
2 weeks to months post-infarction
Atrial and ventricular aneurysms
Clinical features
Persistent (> 3 weeks post-MI) ST elevation and T-wave inversions
Systolic murmur, S3 and/or S4
Diagnosis: echocardiography
Visualization of the pathological myocardial wall protrusion
Detection of dyskinetic movements of the thinned aneurysmal wall (uncoordinated contraction occurs due to fibrotic changes of the myocardium)
Complications
Cardiac arrhythmias (risk of ventricular fibrillation)
Rupture → cardiac tamponade
Mural thrombus formation → thromboembolism (stroke, mesenteric ischemia, renal infarction , acute obstruction of peripheral arteries)
Treatment: anticoagulation, possibly surgery
Postmyocardial infarction syndrome (Dressler syndrome): pericarditis occurring 2–10 weeks post-MI without an infective cause
Thought to be due to circulating antibodies against cardiac muscle cells (autoimmune etiology)
Clinical features
Signs of acute pericarditis: pleuritic chest pain , dry cough , friction rub
Fever
Laboratory findings: leukocytosis, ↑ serum troponin levels
ECG: diffuse ST elevations
Treatment: NSAIDs (e.g., aspirin), colchicine
Complications (rare): hemopericardium, pericardial tamponade
Arrhythmias (e.g., AV block)
Congestive heart failure (e.g., due to ischemic cardiomyopathy)
Can occur at any time after an ischemic event
Treatment: for patients with LVEF < 40% or signs of heart failure, ACE inhibitor/ARB and aldosterone antagonists have been shown to confer a mortality benefit.
Reinfarction
Prevention of ACS and myocardial infarction.
Primary prevention [11]
Treatment/avoidance of modifiable risk factors for atherosclerosis (e.g., smoking cessation, treatment of hypertension, etc.)
Healthy, plant-based diet [41]
Regular physical activity and exercise
Low-dose aspirin is beneficial for certain high-risk groups. The choice to prescribe it should be made on an individual basis.
Secondary prevention [11]
Lifestyle modification and treatment of modifiable risk factors (see “Primary prevention” above and treatment of diseases caused by atherosclerosis)
Platelet-aggregation inhibitors
Lifelong low-dose aspirin 75–100 mg/day
DAPT with the addition of an ADP receptor inhibitor (e.g., prasugrel, ticagrelor, or clopidogrel) is recommended for 12 months for all patients who have undergone PCI.
Glycoprotein IIb/IIIa antagonists (e.g., abciximab) may be considered but are not used routinely.
Beta blockers: Unless contraindicated, all patients should be started on a beta blocker, which has been shown to confer a mortality benefit.
Statin: All patients should be started on a high-intensity statin (e.g., atorvastatin).
An aldosterone antagonist and ACE inhibitor/ARB are recommended for all patients with ischemic cardiomyopathy and an LV ejection fraction < 40% or symptoms of heart failure.
Arrhythmias and Conduction Defects (atrial fibrillation, ).
D: Atrial fibrillation (Afib) is a commonly seen type of supraventricular tachyarrhythmia that is characterized by uncoordinated atrial activation resulting in an irregular ventricular response.
R:
Remember PARASITE to memorize the major risk factors for acute Afib: P – Pulmonary disease; A – Anemia; R – Rheumatic heart disease; A – Atrial myxoma; S – Sepsis; I – Ischemia; T – Thyroid disease; E – Ethanol.
SMITH: sepsis, mitral valve disease, ischaemic heart disease, thyrotoxicosis and hypertension.
While the exact mechanisms are still poorly understood, associations with a number of cardiac (e.g., valvular heart disease, coronary artery disease) and noncardiac (e.g., hyperthyroidism, electrolyte imbalances) risk factors have been established.
CVS risk factors: advanced age, hypertension, diabetes mellitus, smoking, obesity, sleep apnea.
Intrinsic cardiac disorders: coronary artery disease, valvular heart disease (especially mitral valve disease), congestive heart failure (CHF), pre-excitation tachycardia e.g Wolff-Parkinson-White (WPW) syndrome. Sick sinus syndrome (tachycardia-bradycardia syndrome), cardiomyopathies, pericarditis, congenital channelopathies.
Non-cardiac disorders: Pulmonary disease: COPD, pulmonary embolism, pneumonia. Hyperthyroidism, catecholamine release and/or increased sympathetic activity: stress: sepsis, hypovolemia, post-surgical state (especially following cardiac surgery), hypothermia. Pheochromocytoma, cocaine, amphetamines. Electrolyte imbalances (hypomagnesemia, hypokalemia). Drugs: adenosine, digoxin. Holiday heart syndrome: irregular heartbeat classically triggered by excessive alcohol consumption, but also sometimes by moderate alcohol consumption, stress, dehydration or lack of sleep. Chronic kidney disease. Approx. 15% of individuals who develop Afib have none of the above mentioned risk factors (idiopathic/lobe Afib).
D: AFib should be differentiated from other supraventricular tachyarrhythmias with a narrow QRS complex. See supraventricular arrhythmias in the overview section of cardiac arrhythmias.
E: Most common sustained arrhythmia
Incidence: increases with age
The lifetime risk of Afib among individuals > 40 years is 1 in 4.
>95% of individuals with Afib are ≥ 60 years
Prevalence: ∼ 1% of US population.
A:
C: Individuals with Afib are typically asymptomatic. However, when symptoms do occur, these usually include palpitations, lightheadedness, and shortness of breath. Physical examination typically reveals an irregularly irregular pulse.
P:
I:
M: The general principles of treating atrial fibrillation include:
Correcting reversible causes and/or treatable conditions (e.g., hyperthyroidism, electrolyte imbalances)
Controlling heart rate and/or rhythm
Providing anticoagulation.
Anticoagulation is commonly indicated for thrombus prevention and/or breakdown before and after conducting cardioversion. Because AF causes the atria contract rapidly but ineffectively and in an uncoordinated fashion, the resulting stasis of blood may lead to thrombus formation within the atria (especially the left atrial appendage). The sudden restoration of effective atrial contraction following cardioversion may cause a pre-existing thrombus to dislodge, resulting in a thromboembolic event (e.g., stroke, renal infarct).
Unstable AF: emergent electrical cardioversion
Stable AF: rate control or rhythm control strategies to control AF and prevent long-term recurrence.
In stable patients, treatment involves the correction of modifiable risk factors, rate or rhythm control strategies, and anticoagulation. Rate control therapy typically involves the use of beta-blockers or nondihydropyridine calcium channel blockers. Rhythm control strategies involve elective synchronized cardioversion and/or the use of antiarrhythmics (e.g., flecainide, propafenone, or amiodarone). The need for anticoagulation therapy is determined based on the CHA2DS2-VASc score. Catheter-directed or surgical ablation of the arrhythmogenic tissue is used in refractory or severe Afib.
P: Ineffective atrial emptying as a result of Afib can lead to stagnation of blood and clot formation in the atria, which in turn increases the risk of stroke and other thromboembolic complications.
atrial flutter,
A supraventricular tachyarrhythmia usually caused by a single macroreentrant rhythm within the atria that is classically characterized on ECG by the sawtooth appearance of P waves, also known as “flutter waves”, with narrow QRS complexes. Atrial flutter is another type of commonly seen supraventricular tachyarrhythmia that is usually caused by a single macroreentrant rhythm within the atria. The risk factors for atrial flutter are similar to those of Afib. In atrial flutter, the atrial rate is slower than in Afib and the ventricular rhythm is usually regular. Treatment is similar to that of Afib, consisting of anticoagulation and strategies to control heart rate and rhythm. Atrial flutter frequently degenerates into atrial fibrillation.
Epidemiology
Incidence: 88 per 100,000 person-years (increases with age)
Sex: ♂ > ♀ (5:2)
Etiology: similar to atrial fibrillation (see “Etiology” above)
Pathophysiology
Type I (common; typical or isthmus-dependent flutter): caused by a counterclockwise (more common) or clockwise (less common) macroreentrant activation of cardiac muscle fibers in the right atrium that travels along the tricuspid annulus and passes through the cavotricuspid isthmus
Type II (rare, atypical atrial flutter): various reentrant rhythms that do not involve the cardio-tricuspid isthmus, are not well defined, and/or occur in the left atrium
Clinical features
Most patients are asymptomatic
Less commonly, symptoms of arrhythmias such as palpitations, dizziness, syncope, fatigue, and or dyspnea
Symptoms of the underlying disease (e.g., murmurs of mitral stenosis)
Tachycardia with a regular pulse
Diagnostics: similar to atrial fibrillation; see “Diagnostics” above
Sawtooth appearance of P waves: identical flutter waves (F waves) that occur in sequence at a rate of ∼ 300 bpm
Regular, narrow QRS complexes
The rhythm may be:
Regularly irregular if atrial flutter occurs with a variable AV block occurring in a fixed pattern (2:1 or 4:1)
Irregularly irregular with a variable block occurring in a nonfixed pattern
Treatment: similar to atrial fibrillation (see “Therapy” below)
Complications
Frequently degenerates into atrial fibrillation (see “Clinical features” above)
1:1 conduction leading to life-threatening ventricular tachycardia.
Heart block -Dr Deac Pimp
Atrioventricular (AV) block (often referred to as “heart block) involves the partial or complete interruption of impulse transmission from the atria to the ventricles. This interruption of impulse transmission results in characteristic ECG findings that different depending on the sub-type of AV block. The commonest cause of AV block overall is idiopathic fibrosis and sclerosis of the conduction system.
Any patient presenting with possible AV block would require a number of investigations to identify possible underlying causes including:
ECG – to help determine the subtype of AV block Blood tests (e.g. FBC, U&Es, TSH, Troponin) – to rule out underlying causes Echocardiogram – to rule out structural heart disease. Some forms of AV block can be managed conservatively, whereas other sub-types require intervention.
Different types of blocks include: First-degree AV block Second-degree AV block (type 1) Second-degree AV block (type 2) Third-degree (complete) AV block
Third degree, complete heart block.
Third-degree (complete) AV block occurs when there is no electrical communication between the atria and ventricles due to a complete failure of conduction.4
Typical ECG findings include the presence of P waves and QRS complexes that have no association with each other, due to the atria and ventricles functioning independently.
Cardiac function is maintained by a junctional or ventricular pacemaker.4
Narrow-complex escape rhythms (QRS complexes of <0.12 seconds duration) originate above the bifurcation of the bundle of His. A typical heart rate would be >40bpm.
Broad-complex escape rhythms (QRS complexes >0.12 seconds duration) originate from below the bifurcation of the bundle of His. These escape rhythms produce slower, less reliable heart rates and more significant clinical features (e.g. heart failure, syncope).
Aetiology of complete heart block:
Congenital: Structural heart disease (e.g transposition of the great vessels) Autoimmune (e.g maternal SLE) Idiopathic fibrosis: Lev’s disease (fibrosis of the distal His-Purkinje system in the elderly) Lenegre’s disease (fibrosis of the proximal His-Purkinje system in younger individuals) Ischaemic heart disease: Myocardial infarction Ischaemic cardiomyopathy Non-ischaemic heart disease: Calcific aortic stenosis Idiopathic dilated cardiomyopathy Infiltrative disease (e.g sarcoidosis, amyloidosis) Iatrogenic: Post ablative therapies and pacemaker implantation Post cardiac surgery Drug-related: Digoxin Beta-blockers Calcium channel blockers Amiodarone Infections: Endocarditis Lyme disease Chagas’ disease Autoimmune conditions: SLE Rheumatoid arthritis Thyroid dysfunction
ECG findings of complete heart block, clinical features: history, clinical examination, management and complications.
Rhythm: variable
P wave: present but not associated with QRS complexes
PR interval: absent (as there is atrioventricular dissociation)
QRS complex: narrow (<0.12 seconds) or broad (>0.12 seconds)
Depending on the site of the escape rhythm (see introduction).
Clinical features
History
Palpitations
Pre-syncope/syncope
Confusion
Shortness of breath (due to heart failure)
Chest pain
Sudden cardiac death
Clinical examination
Irregular pulse
Profound bradycardia
Haemodynamic compromise (e.g. prolonged capillary refill time and hypotension)
Management
Patients should be placed on a cardiac monitor
Transcutaneous pacing/temporary pacing wire or isoprenaline infusion may be required
Some rhythms (particularly narrow-complex escape rhythms) may respond to atropine
A permanent pacemaker is generally required
Complications
Ventricular arrhythmias leading to sudden cardiac death.
Ventricular tachycardia -Dr Deac Pimp
Definition: Ventricular tachycardia (VT) is a potentially life-threatening arrhythmia originating in the cardiac ventricles. Usually, VT results from underlying cardiac diseases such as myocardial infarction or cardiomyopathy, but it can also be idiopathic or iatrogenic. Clinical manifestations range from palpitations and syncope to cardiogenic shock and sudden cardiac death. The characteristic ECG findings of VT are broad QRS complexes (> 120 ms) and tachycardia (> 120 bpm). In the acute setting, management of VT may require immediate cardioversion, defibrillation, or administration of antiarrhythmic drugs. Most patients who develop symptomatic, sustained VT require long-term antiarrhythmic therapy involving medication, intracardiac devices, or catheter ablation.
Aetiology:
Cardiac scars (usually due to infarction; also iatrogenic, e.g., postoperative)
Conduction disorders
Drugs (e.g., digitalis, antiarrhythmics)
Long-QT syndrome
Congenital long-QT syndrome
Acquired long-QT syndrome
Drugs
Antiarrhythmics
Class Ia (e.g., quinidine, disopyramide)
Class III (e.g., sotalol, amiodarone)
Antibiotics (e.g., macrolides, fluoroquinolones)
Antidepressants (most tricyclic and tetracyclic antidepressants, lithium)
Antipsychotics (e.g., haloperidol)
Anticonvulsants (fosphenytoin, felbamate)
Electrolyte imbalances (hypokalemia, hypomagnesemia, hypocalcemia)
Ischemic stroke or intracranial hemorrhage
Endocrine disorders (e.g., hypothyroidism)
Nutritional disorders (e.g., anorexia nervosa)
In rare cases, VT can occur in healthy individuals.
Pathophysiology:
Monomorphic VT (all QRS complexes look similar)
Increased automaticity
Re-entry circuit
Polymorphic VT (dissimilar QRS complexes): caused by abnormal ventricular repolarization (e.g., long QT syndrome, drug toxicity, electrolyte abnormalities)
Decreased cardiac output: asynchronous atrial and ventricular beats + rapid ventricular rhythm → ↓ blood flow into the ventricle during diastole → ↓ CO
→ hemodynamic compromise → symptoms of syncope, MI, angina.
Clinical features: Often asymptomatic, especially if nonsustained Common symptoms of sustained VT include: Palpitations Hypotension Syncope In more severe cases: Chest pain/pressure (often in conjunction with MI) Cardiogenic shock Loss of consciousness Progression to ventricular fibrillation Sudden cardiac death.
Investigations:
3 or more consecutive premature ventricular beats (i.e., widened QRS)
Heart rate > 120 bpm
Duration
Nonsustained: < 30 s
Sustained: > 30 s
Morphology
Monomorphic: all QRS complexes look similar (identical origin)
Polymorphic: QRS complexes are different (multiple origins)
Other possible ECG findings
AV-dissociation: no relationship between P waves and QRS complexes (in VT, ventricular rhythm is often faster than atrial rhythm)
Fusion complex: atrial and ventricular impulses occur simultaneously
Capture beats: Occasionally, a supraventricular impulse may reach AV node and produce a subsequent ventricular beat (similar to a beat in sinus rhythm).
Other diagnostic tests
Holter monitor: useful for diagnosing intermittent VT which may not be present on a single ECG
Patient-activated (manual) event recorder
Echocardiography: provides information about possible etiologies of VT (e.g. structural heart disease, prior MI) and is thus a useful tool for evaluation of VT.
Differential diagnosis:
Confirming the diagnosis of VT can be challenging and, in some cases, impossible. However, VT accounts for nearly 80% of wide-complex tachycardias.
Supraventricular tachycardia with aberrancy (RBBB, LBBB, Wolff-Parkinson-White)
It is important to make the distinction between SVT with aberrancy and VT because treatment of the two conditions differs and sometimes the wrong treatment can lead to hemodynamic instability (e.g., using AV-nodal blocking drugs in patient with VT).
Signs and symptoms that suggest VT rather than SVT are:
Age > 35 (high PPV)
History of structural heart defects or past MI
AV dissociation, fusion beats, and capture beats
Signs and symptoms that suggest SVT with aberrancy rather than VT are:
Bundle branch block on prior ECG
History of SVT
Evidence of WPW (e.g., delta wave)
If there is any doubt regarding the diagnosis, assume VT rhythm and treat accordingly.
Treatment:
Initial therapy
If patient is hemodynamically unstable (hypotension, loss of consciousness):
VT with pulse → cardioversion
VT without pulse → defibrillation
See “Advanced cardiac life support”
If patient is hemodynamically stable:
Antiarrhythmics (typically lidocaine, procainamide, amiodarone)
Cardioversion if medical therapy fails
In all patients, look for and address possible causes of VT such as:
Electrolyte abnormalities (e.g., hypokalemia) → correct any electrolyte imbalances
Medication-induced QT prolongation → remove any offending medication, digoxin immune fab (fragment antigen-binding) for digoxin toxicity
Long-term therapy
Intracardiac devices (ICD) (most effective treatment for reducing mortality): indicated in case of VT that does not respond to therapy
Catheter ablation
Antiarrhythmics (usually class I or III).
Acute pulmonary oedema-Dr Deac Pimp
Pulmonary oedema occurs when fluid accumulates in the parenchyma and air spaces in the lungs. It is most commonly caused by heart failure or fluid overload.
Clinical features: Symptoms MAIN SYMPTOM: SEVERE DYSPNEA Shortness of breath Respiratory distress Production of pink frothy sputum (haemoptysis) Signs Pallor Tachypnoea Decreased oxygen saturations Raised jugular venous pressure (JVP) Peripheral oedema. -their tactile fremitus is possibly increased, percussion dull, auscultation: fine or coarse crackles, depending on severity, no tracheal deviation.
You will come across acute left ventricular failure often during your medical jobs. This occurs when the left ventricle is unable to adequately move blood through the left side of the heart and out into the body. This causes a backlog of blood (like too many buses waiting to pick up people at a bus stop) that increases the amount of blood stuck in the left atrium, pulmonary veins and lungs. As the vessels in these areas are engorged with blood due to the increased volume and pressure they leak fluid and are unable to reabsorb fluid from the surrounding tissues. This causes pulmonary oedema, which is where the lung tissues and alveoli become full of interstitial fluid. This interferes with the normal gas exchange in the lungs, causing shortness of breath, oxygen desaturation and the other signs and symptoms.
Risk factors/triggers: Iatrogenic (e.g. aggressive IV fluids in frail elderly patient with impaired left ventricular function) Sepsis Myocardial Infarction Arrhythmias
Management: Intravenous opiates (opiates such as morphine act as vasodilators but are not routinely recommended).
Non-Invasive Ventilation (NIV). Continuous Positive Airway Pressure (CPAP) involves using a tight fitting mask to forcefully blow air into their lungs. This helps to open the airways and alveoli to improve gas exchange. If NIV does not work they may need full intubation and ventilation.
“Inotropes”, for example an infusion of noradrenalin. Inotropes strengthen the force of heart contractions and improve heart failure, however they need close titration and monitoring, so by this point you would need to send the patient to the local coronary care unit / high dependency unit / intensive care unit.
Pulmonary oedema causes, symptoms, diagnosis, treatment, pathology.
Pulmonary oedema: build up of fluid in lungs and airways e.g alveoli, and interstitium. Space is mostly filled with proteins, when it fills up with fluid, it can make it hard for oxygen to cross over from the alveoli into the capillary. This leaves the body hypoxic/deprived of oxygen. The two factors hydrostatic pressure and oncotic pressure oppose each other. Capillary permeability of pulmonary arteries also a factor. All 3 of these factors keep the lungs free of excess fluid,.
The underlying cause of pulmonary oedema can be cardiogenic: it develops as a result of heart disease, or it can be non-cardiogenic: damage is to the pulmonary capillaries or alveoli.
The most common cardiogenic cause is left sided heart failure. In this, the left ventricle becomes unhealthy and can’t pump effectively. This means that blood starts to back up into the left atrium, and then the pulmonary veins and pulmonary capillaries. The extra blood in the pulmonary capillaries causes pulmonary hypertension which is an increase in the hydrostatic pressure of the pulmonary blood vessels. This pushes more fluid into the interstitial space of the lungs which leads to pulmonary oedema.
Another cardiogenic cause is severe systemic hypertension, this is greater than 180 systolic and 110 diastolic. In this situation the left ventricle is healthy but can’t effectively pump blood in a system with such a high afterload. Or under conditions with such high systemic pressures. This means that blood starts to back up in the left atrium, pulmonary veins and pulmonary capillaries.This ultimately then leads to pulmonary hypertension and pulmonary oedema.
Non cardiogenic causes of pulmonary oedema include pulomnary infections, inhalation of toxic substances, and trauma to the chest. All of these can cause direct injury to the alveoli. If this happens there is usually an inflammatory process that makes nearby capillaries more permeable. As a result, proteins and fluid enter the interstitial space. Another cause is sepsis, A key difference is that sepsis is when inflammation happens throughout the body, rather than just in the lungs. So in addition to pulmonary oedema, sepsis can cause extra fluid in the interstitial space of fluids throughout the body. Another cause is having low oncotic pressure, this can result from not making enough proteins, such as albumin, due to malnutrition or from liver failure.
Alternatively it can be due to losing protein too quickly, as in nephrotic syndrome. Regardless of the cause, low oncotic pressure causes fluid from capilliary to enter into the interstitial space of the body. In the lungs this results in pulmonary oedema.
Pulmonary oedema now makes gas exchange difficult because oxygen and carbon dioxide have to diffuse through a wide layer of interstitial fluidm to get from alveoli to pulmonary capillary and vice versa. That journey CAN also take too long relative to blood moving through the lungs. tHIS MAKES IT hard to fully oxygenate the blood. Pulmonary oedema can lead to severe shortness of breath, and in left sided heart failure it can lead to orthopnea, which is when there is worse shortness of breath when lying flat. this happens because there is increased pulmonary congestion when lying down. In left sided ventricular heart failure, the pulmonary circulation is already overloaded, as a result the extrablood can’t be pumped out efficiently, and it causes shortness of breath.
This pumonary congestion and shortness of breath decrease when a person sits up.
Diagnosis: made with a chest x-ray or a chest CT scan. This shows fluid in the interstitial space.
Treatment for pulmonary oedema involves giving supplemental oxygen, other treatments are dependent on the underlying cause. If the cause is cardiogenic in nature then medications aimed at boosting hearts performance or lowering blood pressure can be helpful. If the cause is related to inflammation or low oncotic pressure, then managing that illness will help resolve the pulmonary oedema.
Hypertension Dr deac pimp
D: Hypertension is a common condition that affects one in every three adults in the United States. The AHA/ACC guidelines define it as a blood pressure of ≥ 130/80 mm Hg and by JNC 8 criteria as ≥ 140/90 mm Hg. Hypertension can be classified as either primary (essential) or secondary. Primary hypertension accounts for approx. 95% of cases of hypertension and has no detectable cause, whereas secondary hypertension is due to a specific underlying condition.
R:
Ddx: Typical underlying conditions include renal, endocrine, or vascular diseases (e.g., renal failure, primary hyperaldosteronism, or coarctation of the aorta).
Hypertension:
Diagnostic findings and underlying conditions:
-Hypokalemia–> underlying condition: Conn syndrome, renal artery stenosis.
-Metabolic alkalosis and increase aldosterone to renin ratio–> underlying condition Conn syndrome.
-Difference in blood pressure:
1. In both arms: takayasu arteritis, aortic dissection, aortic arch syndrome, subclavian steal syndrome.
2. Of upper and lower limbs: coarctation of the aorta distal to the left subclavian artery.
-Daytime sleepiness (Epworth scale, Berlin questionnaire), Nondipping (“Nondipping” is a term used to describe the failure of blood pressure to fall by 10% or more during sleep. Patients who show this pattern are often referred to as “nondippers.”) in 24-hour blood pressure monitoring: obstructive sleep apnea.
-Increased 24-hour urinary metanephrines: pheochromocytoma.
-Increase serum calcium, increase PTH level, decrease serum phosphates: hyperparathyroidism.
-increase serum cortisol: excess of glucocorticoids (e.g Cushing syndrome).
-Decrease TSH, increase free T4.
E: Prevalence
One in three adults in the US is affected.
Prevalence increases with age (∼ 65% among those ≥ 60 years of age).
African Americans are more commonly affected than Asian American or white individuals.
60–75% of obese and overweight patients are affected.
Sex: ♂ > ♀ below age of 45; the sex ratio is almost balanced at > 45 years of age (i.e., after menopause)
Most common risk factor for cardiovascular disease
A: Primary (essential) hypertension
No specific cause; multifactorial etiology including epigenetic/genetic and environmental factors
Accounts for 85–95% of cases of hypertension in adults
Accounts for 15–20% of cases of hypertension in children < 12 years of age
Age at onset: 25–55 years (prevalence is increasing in adolescents)
Risk factors
Nonmodifiable risk factors
Positive family history
Ethnicity
Advanced age
Modifiable risk factors
Obesity
Diabetes
Smoking, excessive alcohol or caffeine intake
Diet high in sodium, low in potassium
Physical inactivity
Psychological stress
Secondary hypertension
Caused by an identifiable underlying condition
Accounts for 5–15% of cases of hypertension in adults
Accounts for 70–85% of cases of hypertension in children < 12 years of age
Age at onset < 25 years or > 55 years
Causes
Endocrine hypertension
Primary hyperaldosteronism (Conn syndrome): most common cause of secondary hypertension in adults
Hypercortisolism (Cushing syndrome)
Hyperthyroidism
Pheochromocytoma
Primary hyperparathyroidism
Acromegaly
Congenital adrenal hyperplasia
Renal hypertension
Renovascular hypertension (e.g., due to renal artery stenosis)
Polycystic kidney disease (ADPKD)
Renal failure (renal parenchymal hypertension)
Glomerulonephritis
Systemic lupus erythematosus
Renal tumors
Coarctation of the aorta
Obstructive sleep apnea
Medication: sympathomimetic drugs, corticosteroids, NSAIDs, oral contraceptives
Recreational drug use: amphetamines, cocaine, phencyclidine
Isolated systolic hypertension: See “subtypes and variants” below for details.
RECENT can help you remember the causes of secondary hypertension: R = Renal (e.g., renal artery stenosis, glomerulonephritis), E = Endocrine (e.g., Cushing syndrome, hyperthyroidism, Conn syndrome), C = Coarctation of aorta, E = Estrogen (oral contraceptives), N = Neurologic (raised intracranial pressure, psychostimulants use), T = Treatment (e.g., glucocorticoids, NSAIDs).
C: Clinically, hypertension is usually asymptomatic until organ damage occurs, which then commonly affects the brain, heart, kidneys, or eyes (e.g., retinopathy, myocardial infarction, stroke). Common early symptoms of hypertension include headache, dizziness, tinnitus, and chest discomfort.
Hypertension is usually asymptomatic until:
Complications of end-organ damage arise (see “Complications” below)
Or an acute increase in blood pressure occurs (see hypertensive crisis below)
Secondary hypertension usually manifests with symptoms of the underlying disease (e.g., abdominal bruit in renovascular disease, edema in CKD, daytime sleepiness in obstructive sleep apnea).
Nonspecific symptoms of hypertension
Headaches, esp. early morning or waking headache
Dizziness, tinnitus, blurred vision
Flushed appearance
Epistaxis
Chest discomfort, palpitations; strong, bounding pulse on palpation
Nervousness
Fatigue, sleep disturbances.
P:
I: Hypertension is diagnosed if blood pressure is persistently elevated on two or more separate measurements. Further diagnostic measures include evaluation of possible organ damage (e.g., kidney function tests) and additional tests if an underlying disease is suspected.
General approach
Blood pressure monitoring
Repeated measurements on both arms : Hypertension is diagnosed if the average blood pressure on at least two readings obtained on at least two separate visits is elevated.
Long-term measurement of blood pressure (24 hours)
See “Blood pressure measurement” for the basic approach to measurement.
Initial evaluation of newly diagnosed hypertensive patients
Stratification of cardiovascular risk: fasting blood glucose, lipid profile (HDL, LDL, and triglycerides levels)
Evaluation of end-organ damage and underlying causes
Complete blood count
Renal function tests: serum creatinine and eGFR
Serum Na+, K+, and Ca2+
Urinalysis
TSH
Electrocardiogram (ECG)
Approach to diagnosing secondary hypertension
General indicators of secondary hypertension
Young age (< 30 years) at onset of hypertension
Onset of diastolic hypertension at an older age (> 55 years)
Abrupt onset of hypertension
End-organ damage that is disproportionate to the degree of hypertension
Recurrent hypertensive crises
Resistant hypertension: hypertension that is resistant to treatment with at least three antihypertensives of different classes including a diuretic
Specific indicators (For details regarding individual diagnostic procedures, see the individual articles.)
Screening for hypertension (USPSTF recommendations) [36]
Individuals 18–39 years of age with normal blood pressure (< 130/85 mm Hg) and without other risk factors: Screen every 3–5 years.
Individuals > 40 years of age or who are at increased risk for high blood pressure : Screen every year.
M: Treatment of primary hypertension includes lifestyle changes (e.g., diet, weight loss, exercise) and pharmacotherapy. Commonly prescribed antihypertensive medications include ACE inhibitors, angiotensin receptor blockers, thiazide diuretics, and calcium channel blockers. Management of pediatric patients and pregnant women differs from that of nonpregnant adults because some of these drugs are contraindicated in these patient groups. To treat secondary hypertension, the underlying cause needs to be addressed.
Initiation of treatment
Number of antihypertensives
Newly diagnosed hypertension with BP < 150/90 mm Hg: Begin therapy with one primary antihypertensive.
Newly diagnosed hypertension with BP > 150/90 mm Hg: Begin therapy with two primary antihypertensives.
Choice of antihypertensive drug
Non-African American patients (including individuals with diabetes): thiazide-type diuretic, calcium channel blocker (CCB), angiotensin-converting enzyme inhibitor (ACE-I), or angiotensin receptor blocker (ARB)
African American patients (including individuals with diabetes): thiazide-type diuretic or CCB
In adults with chronic kidney disease: initial (or add-on) treatment should include an ACE inhibitor or ARB to improve kidney outcome.
Follow-up
Reassess within one month of initiating or changing pharmacological therapy.
If the treatment goal is not reached with one drug, increase the dose of the initial drug or add a second drug.
If the treatment goal cannot be reached with two drugs:
Add a third drug.
Evaluate for secondary causes of hypertension.
If blood pressure is controlled: Reassess after 3–6 months and annually thereafter.
Overview of antihypertensive drugs:
First-line drugs:
-ACE inhibitors (e.g lisinopril, captopril, enalapril) and Angiotensin-receptor blockers (e.g losartan, valsartan) -Preferred as a first-line drug in patients with diabetes mellitus, renal disease (nephroprotective), ischemic heart disease, and heart failure
ACEi and ARBs should not be used in combination.
-Angiotensin-receptor blockers (ARB)(e.g, losartan, valsartan).
-Thiazide diuretics (e.g hydrochlorothiazide, chlorthalidone)
-Calcium channel blockers.
Treatment of hypertension in pregnancy:
Treatment of hypertension in pregnancy
First-line treatment: methyldopa , labetalol, hydralazine (vasodilator), and nifedipine (CCB)
Second-line treatment: thiazides, clonidine (alpha-2 agonist)
Contraindicated: furosemide, ACE-I, ARB, renin inhibitors (aliskiren)
For details, see treatment of gestational hypertension.
Treatment of hypertension in children
Treat the underlying cause (e.g., surgical correction of coarctation of the aorta)
Lifestyle changes in children with elevated BP (see nonpharmacologic measures in the treatment section below)
Pharmacologic management is indicated for symptomatic hypertension, diabetes mellitus, CKD, and end-organ damage, as well as if there is an insufficient response or no response to lifestyle changes.
Goal: BP < 90th percentile (BP < 50th percentile in children with DM or CKD)
Drugs: ACE inhibitor, ARB, or calcium channel blocker
In children with CKD or diabetes mellitus, ACE inhibitors or ARBs are preferable.
Hypertensive emergency: labetalol, nicardipine, or sodium nitroprusside.
Beta blockers are not recommended for initial treatment of hypertension in children due to their metabolic side effects (e.g., impaired glucose tolerance) and the fact that they exacerbate asthma!
P/C: -Arterial hypertension leads to changes in the vascular endothelium, particularly of the small vessels, and can therefore affect any organ system. See also hypertensive crises. Cardiovascular system Congestive heart failure, dilated cardiomyopathy, hypertrophic cardiomyopathy Coronary artery disease and myocardial infarction Atrial fibrillation Aortic aneurysm Aortic dissection Carotid artery stenosis Peripheral artery disease Atherosclerosis
Brain:
Stroke , TIA
Cognitive changes such as memory loss.
Kidneys
Hypertensive nephrosclerosis
Pathophysiology: chronic hypertension → narrowing of afferent arterioles and efferent arterioles → reduction of glomerular blood flow → glomerular and tubular ischemia → arteriolonephrosclerosis and fibrosis (focal segmental glomerulosclerosis) → end-stage renal disease
Typical findings
Initially microalbuminuria and microhematuria
With disease progression, nephrosclerosis with macroalbuminuria (usually < 1 g/day) and progressive renal failure occur.
Biopsy: sclerosis in capillary tufts, arterial hyalinosis
Eyes
Hypertensive retinopathy
Arteriosclerotic and hypertension-related changes of the retinal vessels
Fundoscopic examination:
Cotton-wool spots
Retinal hemorrhages (i.e., flame-shaped hemorrhages)
Microaneurysms
Macular star (results from exudation into the macula)
Arteriovenous nicking
Marked swelling and prominence of the optic disk with indistinct borders due to papilledema and optic atrophy (end-stage disease)
Presence of papilledema in a hypertensive patient may indicate a hypertensive crisis and warrants urgent lowering of the blood pressure (see hypertensive crises).
Local treatment of the eye is not possible; therefore, systemic reduction of blood pressure is critical!
Subtypes and variants of hypertension
White coat hypertension:
Definition: arterial hypertension detected only in clinical settings or during blood pressure measurement at a physician’s practice
Etiology: anxiety experienced by the patient
Clinical features: consistently normal blood pressure measurements and normalization of elevated blood pressure outside of a clinical setting
Diagnostics: 24-hour blood pressure monitoring.
Isolated systolic hypertension (ISH)
Definition: increase in systolic blood pressure (≥ 140 mm Hg) with diastolic BP within normal limits (≤ 90 mm Hg)
Etiology
ISH in elderly: decreased arterial elasticity and increased stiffness → decreased arterial compliance
ISH secondary to increased cardiac output
Anemia
Hyperthyroidism
Chronic aortic regurgitation
AV fistula
Clinical features:
Often asymptomatic
Signs of increased pulse pressure: e.g., head pounding, rhythmic nodding, or bobbing of the head in synchrony with heartbeats
Symptoms of hypertension (see “clinical features” above)
Diagnostics: See “diagnosis of hypertension” below.
Treatment: thiazide diuretics or dihydropyridine calcium antagonists
Prognosis: high risk of cardiovascular events (MI, stroke, renal dysfunction).
Congestive heart failure
D: Congestive heart failure (CHF) is a clinical condition in which the heart is unable to pump enough blood to meet the metabolic needs of the body because of pathological changes in the myocardium.
Congestive heart failure (CHF): a clinical syndrome in which the heart is unable to pump enough blood to meet the metabolic needs of the body; characterized by ventricular dysfunction that results in low cardiac output
Systolic dysfunction: CHF with reduced stroke volume and ejection fraction (EF)
Diastolic dysfunction: CHF with reduced stroke volume and preserved ejection fraction
Right heart failure (RHF): CHF due to right ventricular dysfunction; characterized by backward heart failure
Left heart failure (LHF): CHF due to left ventricular dysfunction; characterized by forward heart failure
Biventricular (global) CHF: CHF in which both the left and right ventricle are affected, resulting in simultaneous backward and forward CHF
Chronic compensated CHF: clinically compensated CHF; the patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable (see “Diagnostics” below)
Acute decompensated CHF: sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition (e.g., myocardial infarction)
R: Obesity
Smoking
COPD
Heavy drug (recreational and prescription) and alcohol abuse
D:
E: revalence
1–2% of the population (∼ 5.7 million individuals) in the US has CHF.
The incidence is higher among African Americans, Hispanics, and Native Americans.
Increases with age: ∼ 10% of individuals > 60 years old are affected.
Systolic heart disease is the most common form of CHF overall.
A: The three main causes of CHF are coronary heart disease, diabetes mellitus, and hypertension. These conditions cause ventricular dysfunction with low cardiac output, which results in blood congestion (backward failure) and poor systemic perfusion (forward failure).
General causes:
-systolic dysfunction (reduced EF) & Diastolic dysfunction (preserved EF):
Coronary artery disease, myocardial infarction
Arterial hypertension
Valvular heart disease
Diabetes mellitus (diabetic cardiomyopathy)
Renal disease
Infiltrative diseases (e.g., hemochromatosis, amyloidosis).
Specific causes:
-systolic dysfunction (reduced EF)
Cardiac arrhythmias
Dilated cardiomyopathy (e.g., Chagas disease, chronic alcohol use, idiopathic)
Myocarditis
-diastolic dysfunction (Constrictive pericarditis
Restrictive or hypertrophic cardiomyopathy
Pericardial tamponade).
C: CHF is classified as either left heart failure (LHF) or right heart failure (RHF), although biventricular (global) CHF is most commonly seen in clinical practice. LHF leads to pulmonary edema and resulting dyspnea, while RHF induces systemic venous congestion that causes symptoms such as pitting edema, jugular venous distension, and hepatomegaly. Biventricular CHF manifests with clinical features of both RHF and LHF, as well as general symptoms such as tachycardia, fatigue, and nocturia. In rare cases, high-output CHF may occur as a result of conditions that increase cardiac output and thereby overwhelm the heart. Acute decompensated heart failure (ADHF) may occur as an exacerbation of CHF or be caused by an acute cardiac condition such as myocardial infarction. CHF is diagnosed based on clinical presentation and requires an initial workup to assess disease severity and possible causes. Initial workup includes measurement of brain natriuretic peptide levels, chest x-ray, and an ECG.
P: Cardiac output, which is stroke volume times heart rate, is determined by three factors: preload, afterload, and ventricular contractility.
Underlying mechanism of reduced cardiac output
Systolic ventricular dysfunction (most common) due to:
Reduced contractility: Damage and loss of myocytes reduce ventricular contractility and stroke volume.
Increased afterload: increase in mean aortic pressure, outflow obstruction
Increased preload: ventricular volume overload
Cardiac arrhythmias
High-output conditions (see “High-output heart failure” below)
Diastolic ventricular dysfunction due to:
Decreased ventricular compliance: increased stiffness or impaired relaxation of the ventricle → reduced ventricular filling and increased diastolic pressure → decreased cardiac output
Increased afterload: increase in pulmonary artery pressure
Increased preload: ventricular volume overload
Consequences of systolic and diastolic dysfunction
Forward failure: reduced cardiac output → poor organ perfusion → organ dysfunction (e.g., hypotension, renal dysfunction)
Backward failure
Increased left-ventricular volume and pressure → backup of blood into lungs → increased pulmonary capillary pressure → cardiogenic pulmonary edema
Reduced cardiac output → systemic venous congestion → edema and progressive congestion of internal organs
Resulting macroscopic findings: nutmeg liver
Compensation mechanisms
Aim: maintain cardiac output if stroke volume is reduced
↑ Adrenergic activity → increase in heart rate, blood pressure, and ventricular contractility
Increase of renin-angiotensin-aldosterone system activity (RAAS): activated following decrease in renal perfusion secondary to reduction of stroke volume and cardiac output
↑ Angiotensin II secretion → vasoconstriction → ↑ systemic blood pressure → ↑ afterload
Kidney: vasoconstriction of the efferent arterioles and, to a lesser degree, the afferent arterioles → ↓ net renal blood flow and ↑ intraglomerular pressure to maintain GFR
↑ Aldosterone secretion → ↑ renal Na+ and H2O resorption → ↑ preload
Brain natriuretic peptide (BNP): ventricular myocyte hormone released in response to increased ventricular filling and stretching
↑ Intracellular smooth muscle cGMP → vasodilation → hypotension and decreased pulmonary capillary wedge pressure.
I:
Heart failure is primarily a clinical diagnosis. Laboratory tests and imaging tests, including a chest x-ray and echocardiogram, are useful for evaluating the severity and cause of the condition.
Diagnostic approach [22]
Medical history, including preexisting conditions and history of alcohol and recreational or prescribed drug use
Initial evaluation involves a range of routine laboratory tests and a test for BNP level, ECG, and chest x-ray.
Echocardiography is the gold standard tool for assessing cardiac morphology and function, as well as investigating the underlying cause of CHF.
Other procedures (exercise testing, angiography) may be required for further investigation.
Initial evaluation [22]
Laboratory analysis
Elevated BNP and NT-pro BNP
High levels of BNP in patients with classic symptoms of CHF confirm the diagnosis (high predictive index).
Elevated atrial natriuretic peptide (ANP):
Complete blood count: may show anemia
Serum electrolyte levels: hyponatremia → indicates a poor prognosis
Kidney function tests: ↑ creatinine, ↓ sodium
Urine analysis: rule out concurrent renal impairment
Fasting glucose: to screen for diabetes mellitus, which is a common comorbidity
Fasting lipid profile: to detect dyslipidemia associated with a higher cardiovascular risk
Electrocardiogram (ECG)
ECG abnormalities in CHF are common, but are mostly nonspecific and nondiagnostic.
Signs of left ventricular hypertrophy
↑ QRS voltage (in the left chest leads and limb leads I and aVL) → positive Sokolow-Lyon index
↑ QRS duration (incomplete or complete left bundle branch block)
Left axis deviation
Assessment of prior or concurrent heart conditions
Previous or acute MI: see ECG changes in STEMI
Arrhythmias (e.g., atrial fibrillation, ventricular arrhythmias, sinus tachycardia or bradycardia, AV block)
Signs of pericardial effusion and tamponade: low voltage ECG
Chest x-ray
Useful diagnostic tool to evaluate a patient with dyspnea and differentiate CHF from pulmonary disease
Signs of cardiomegaly
Cardiac-to-thoracic width ratio > 0.5
Boot-shaped heart on PA view (due to right ventricular enlargement)
Assess pulmonary congestion (see x-ray findings in pulmonary congestion).
Transthoracic echocardiogram
Gold standard for evaluating patients with heart failure
Assess ventricular function and hemodynamics
Atrial and ventricular size
Interventricular septum thickness: > 11 mm (normal 6–11 mm) indicates cardiac hypertrophy
Systolic function: left ventricular ejection fraction
Normal EF: > 55%
Reduced EF: 30–44%
Extremely reduced EF: < 30%
Diastolic function (diastolic filling, ventricle dilation)
Investigate etiology
Valvular heart disease
Wall motion abnormalities (indicate prior or acute MI)
Right ventricular strain
Tissue Doppler: ↑ PCWP in left-sided heart failureTransthoracic echocardiogram
Gold standard for evaluating patients with heart failure
Assess ventricular function and hemodynamics
Atrial and ventricular size
Interventricular septum thickness: > 11 mm (normal 6–11 mm) indicates cardiac hypertrophy
Systolic function: left ventricular ejection fraction
Normal EF: > 55%
Reduced EF: 30–44%
Extremely reduced EF: < 30%
Diastolic function (diastolic filling, ventricle dilation)
Investigate etiology
Valvular heart disease
Wall motion abnormalities (indicate prior or acute MI)
Right ventricular strain
Tissue Doppler: ↑ PCWP in left-sided heart failure.
Further tests
Cardiac stress test (exercise tolerance test): to assess the functional impairment due to CHF or other conditions (particularly CHD!)
Radionuclide ventriculography : indicated to assess left ventricular volume and ejection fraction (LVEF)
Cardiac MRI: particularly useful for assessing cardiac morphology and function
Cardiac size and volumes, wall thickness, valvular defects, wall motion abnormalities
Coronary angiography (left heart catheterization): indicated to detect/confirm CHD and possible percutaneous coronary intervention
Right heart catheterization: if pulmonary hypertension is suspected, to assess the severity of systolic dysfunction, and/or to differentiate between types of shock
SvO2: will be low in decompensated heart failure
Endomyocardial biopsy: may be performed if a specific diagnosis is suspected in patients with rapidly progressive clinical CHF or in case the results would alter the management of the patient, e.g., in amyloidosis.
M: Management of CHF includes lifestyle modifications and treatment of associated conditions (e.g., hypertension) and comorbidities (e.g., anemia), along with pharmacologic agents that reduce the workload of the heart. ADHF requires hospitalization and more intensive measures, such as hemodialysis.
General measures [22]
Lifestyle modifications
Salt restriction (< 3 g/day)
Fluid restriction in patients with edema and/or hyponatremia
Weight loss and exercise
Cessation of smoking and alcohol consumption
Immunization: pneumococcal vaccine and seasonal influenza vaccine
Patient education
Self-monitoring and symptom recognition
Daily weight check
Weight gain > 2 kg within 3 days: consult the doctor
Monitoring of potential side effects (e.g., hypotension caused by ACE inhibitors, hyperkalemia caused by aldosterone-antagonists, sensitivity to sunlight caused by amiodarone)
Treat any underlying conditions and contributing comorbidities.
Pharmacologic treatment algorithm
Drugs that improve prognosis: beta blockers, ACE inhibitors, and aldosterone antagonists!
Drugs that improve symptoms: diuretics and digoxin (significantly reduce the number of hospitalizations)!
Conducting regular blood tests to assess electrolyte levels (potassium and sodium) is mandatory if the patient is on diuretics!
Contraindicated drugs
NSAIDs
Worsen renal perfusion (see “Side effects” of NSAIDs)
Reduce the effect of diuretics
May trigger acute cardiac decompensation
Calcium channel blockers (verapamil and diltiazem): negative inotropic effect; worsen symptoms and prognosis
Thiazolidinediones: promote the progression of CHF (↑ fluid retention and edema) and increase the hospitalization rate
Moxonidine: increases mortality in CHF with reduced ejection fraction (systolic dysfunction)
Invasive procedures
Implantable cardiac defibrillator (ICD): prevents sudden cardiac death
Primary prophylaxis indications
CHF with EF < 35% and prior myocardial infarction/CHD
Increased risk of life-threatening cardiac arrhythmias
Secondary prophylaxis indications: history of sudden cardiac arrest, ventricular flutter, or ventricular fibrillation
Cardiac resynchronization therapy (biventricular pacemaker): improves cardiac function
Indications: CHF with EF < 35%, dilated cardiomyopathy, and left bundle branch block
Can be combined with an ICD
Coronary revascularization with PCTA or bypass surgery may be indicated if CAD is present.
Valvular surgery if valvular heart defects are present
Ventricular assist devices: may be implanted to support ventricular function; may be indicated for temporary or long-term support (e.g., to bridge time until transplantation) of decompensated CHF
Cardiac transplantation: for patients with end-stage CHF (NYHA class IV), ejection fraction < 20%, and no other viable treatment options.
P: The prognosis depends on the patient, type and severity of heart disease, medication regimens, and lifestyle changes.
The prognosis for patients with preserved EF is similar to or better than for patients with decreased EF
Risk stratification scales may be used to evaluate the prognosis (e.g., CHARM and CORONA risk scores).
Factors associated with worse prognosis
Elevated BNP
Hyponatremia
Systolic BP < 120 mm Hg
Diabetes
Anemia
Weight loss or underweight
S3 heart sound
Implantable cardioverter-defibrillator use
Frequent hospitalizations due to CHF
1-year survival according to NYHA stage
Stage I: ∼ 95%
Stage II: ∼ 85%
Stage III: ∼ 85%
Stage IV: ∼ 35%.
Complications include: acute decompensated heart failure. Cardiorenal syndrome.
Angina different types:
Angina
Typically retrosternal chest pain or pressure
Pain can also radiate to left arm, neck, jaw, epigastric region, or back.
Pain does not depend on body position or respiration
No chest wall tenderness
Angina may be absent, particularly in younger patients
Often gradual progression
Can also present as gastrointestinal discomfort
Dyspnea
Dizziness, palpitations
Restlessness, anxiety
Autonomic symptoms (e.g., diaphoresis, nausea, vomiting, syncope)
Stable angina
Symptoms are reproducible/predictable
Complaints often subside within minutes , with rest or after administration of nitroglycerin
Common triggers
Mental or physical stress
Exposure to cold
Unstable angina
Symptoms are not reproducible/predictable
Usually occurs at rest or with minimal exertion and is usually not relieved by rest or nitroglycerin
Every new-onset angina
Severe, persistent, and/or worsening angina (crescendo angina)
Increasing intensity, frequency, or duration in a patient with a known stable angina
Unstable angina is a form of acute coronary syndrome and may progress to myocardial infarction. Most patients with CHD first become symptomatic with acute myocardial infarction or sudden cardiac death!
Angina Dr Deac Pimp
D: A narrowing of the coronary arteries reduces blood flow to the myocardium (heart muscle). During times of high demand such as exercise there is insufficient supply of blood to meet demand. This causes symptoms the symptoms of angina, typically constricting chest pain with or without radiation to jaw or arms. Angina is “stable” when symptoms are always relieved by rest or glyceryl trinitrate (GTN). It is “unstable” when the symptoms come on randomly whilst at rest, and this is considered as an Acute Coronary Syndrome. Stable angina (aka Angina Pectoris) is a common presentation of Coronary Heart disease – CHD(aka Ischaemic Heart disease – IHD)
Stable angina, (aka ‘Angina pectoris’, and colloquially “Angina“) is a syndrome which causes exertional chest pain, relieved by either rest or the use of nitrates
Stable angina is a clinical syndrome rather than a disease – and represents a clinical manifestation of underlying coronary artery disease
It occurs when there is insufficient oxygen supply to the heart to meet demand i.e. when there is myocardial ischaemia without infarct
This inability typically occurs as a result of narrowing of the coronary arteries. This narrowing can be due to:
Atherosclerosis
Arterial spasm
(Blood clot – which is the mechanism seen in acute coronary syndromes.
R: The risk factors are the same as for all manifestations of cardiovascular disease:
Hypertension Dyslipidaemia High LDL and low LDL levels Diabetes Obesity FHx of arterial disease Significant if a first degree relative had MI before the age of 55 Smoking Age Male gender
D: It is extremely important to differentiate stable angina from ACS – acute coronary syndrome (unstable angina, NSTEMI and STEMI) – whereby there is an acute narrowing or complete occlusion of the coronary artery due to blood clot – as the treatment is very different. Acute coronary syndrome results in infarction (and death) of myocardial tissue, not just ischaemia. However, the presenting symptom – chest pain – often feels identical to that of ACS – as the mechanism of the pain is essentially the same – lack of oxygen to the heart muscle.
If the pain doesn’t resolve within 5 minutes of cessation of activity, and/or with use of GTN spray, treat as ACS
Angina is typically exertional
Suspicion of ACS should be increased if the symptoms have occurred at rest
MI causes permanent heart muscle damage (infarct), stable angina does not. They have similar symptoms, although the pain of MI is often greater than angina. Any diagnosis of sudden onset chest pain should be treated as ACS until proven otherwise (unless the pain does resolve as above and the patient already has a diagnosis of stable angina).
E: Prevalence of about 3%
This is lower than some other manifestations of cardiovascular disease – such as peripheral vascular disease – which is about 10%
A: Atheroma seen in coronary artery disease – this accounts for the vast majority of cases
Aortic valve disease
Hypertrophic cardiomyopathy
Classifying causes by oxygen supply and demand
Oxygen demand factors – heart rate, blood pressure, left ventricular hypertrophy (more muscle to supply!), valve disease – e.g. aortic stenosis – so the heart has to work harder to pump
Oxygen supply – duration of diastole (needs to be long enough to allow sufficient blood to flow to the heart), coronary vasomotor tone, haemoglobin levels, oxygen saturation.
People normally experience angina as exertional chest pain that is relieved by rest.
People may also experience myocardial ischaemia as shortness of breath or without symptoms (silent ischaemia).
Other precipitating factors
Cold weather
Heavy meals
Intense emotion
C: Angina typically presents as central or left sided chest pain, with or without radiation to the neck, arm or jaw, and is generally transient, most commonly occurring on exertion, but can also be triggered by emotion
Acute attacks are treated with nitrites (e.g. sublingual GTN spray)
It is diagnosed with a combination of history, ECG and myocardial imagining – typically an angiogram
Long-term management involves the use of beta-blockers, calcium-channel blockers, long-acting nitrates, aspirin and statins
Central or left sided chest discomfort
May radiate to the jaw, arm epigastrium – like ACS pain
Can vary from mild to severe
Usually described as a “tight” or “crushing” sensation
Dyspnoea may or may not be present
Usually results from exertion
Symptoms relieved by rest
Symptoms typically of several minutes duration – shorter acting symptoms of a few seconds only are unlikely to be ischaemia related
Patient may get frequent symptoms (several times daily) or only rarely (months between episodes)
This does not necessarily correspond to the severity of the disease
Crescendo angina is said to occur when attacks are increasing in frequency and / or severity and is correlated to high risk of severe ACS
Any changes to a patient’s usual pattern of symptoms should be considered a significant risk for ACS and investigated as such.
P:
I:
Diagnosing Stable Angina
Diagnosing stable angina can be quite tricky. There are several aspects:
Ruling out other causes of chest pain – particularly ACS
Assessing the history as being “typical” for stable angina, with ECG
ECG might be normal, but changes can include:
Pathological Q waves
ST depression
LBBB
T-wave flattening or inversion
Confirming the diagnosis with imaging
Usually CT coronary angiogram (CTCA) is the first line investigation
Consider stress echo or myocardial perfusion scan if this is not available or appropriate
Depending on the severity of the disease detected, patients may be offered angiogram
If very high clinical suspicion you can refer to cardiology without imaging – start treatment first
If low clinical suspicion – consider stress test (ECG or Echo) +/- other cardiac imaging (e.g. CTCA, myocardial perfusion scan) to confirm the diagnosis before referral
Typical History
Chest Pain – is ‘tight’, heavy’, or ‘gripping’.
The pain is usually felt behind the sternum and can radiate to the neck, jaw, arms, and sometimes back.
Shortness of breath (SOB)
Both pain and SOB brought on by exertion, and relieved by rest
Symptoms typically last several minutes after the precipitating event has stopped (e.g. exercise or stress)
Classically relieved by GTN
The likelihood of a diagnosis of angina increases when there are risk factors for cardiovascular disease present:
Smoking Hypertension Diabetes FHx of cardiovascular disease under the age of 55 Raised cholesterol.
Investigations
CT Coronary Angiography is the Gold Standard diagnostic investigation. This involves injecting contrast and taking CT images timed with the heart beat to give a detailed view of the coronary arteries, highlighting any narrowing.
All patients should have to following as baseline investigations:
Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (check for hypo / hyper thyroid)
HbA1C and fasting glucose (for diabetes).
M:
-First thing is to refer to cardiology, and do this urgently if they are having unstable angina, or routinely if stable.
Advise about diagnosis and management and when to call an ambulance.
Treat medically, then do procedures and surgical interventions to treat the underlying stenosis of the coronary arteries.
Medical Management
There are three aims to medical management:
Immediate Symptomatic Relief
Long Term Symptomatic Relief
Secondary prevention of cardiovascular disease
Immediate Symptomatic Relief
Their GTN spray is used required. It causes vasodilation and helps relieves the symptoms.
Take GTN, then repeat after 5 minutes. If there is still pain 5 minutes after the repeat dose – call an ambulance.
Long Term Symptomatic Relief is with either (or used in combination if symptoms are not controlled on one):
Beta blocker (e.g. bisoprolol 5mg once daily) or; Calcium channel blocker (e.g. amlodipine 5mg once daily) Other options (not first line):
Long acting nitrates (e.g. isosorbide mononitrate)
Ivabradine
Nicorandil
Ranolazine
Secondary Prevention
Aspirin (i.e. 75mg once daily)
Atorvastatin 80mg once daily
ACE inhibitor
Already on a beta-blocker for symptomatic relief.
Procedural / Surgical Interventions
Percutaneous Coronary Intervention (PCI) with coronary angioplasty (dilating the blood vessel with a balloon and/or inserting a stent) is offered to patients with “proximal or extensive disease” on CT coronary angiography. This 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 so that the coronary arteries and any areas of stenosis are highlighted on the xray images. This can then be treated with balloon dilatation followed by insertion of a stent.
Coronary Artery Bypass Graft (CABG) surgery may be offered to patients with severe stenosis. This involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis. The recovery is slower and the complication rate is higher than PCI.
TOM TIP: When examining a patient that you think may have coronary artery disease, check for a midline sternotomy scar (previous CABG), scars around the brachial and femoral arteries (previous PCI) and along the inner calves (saphenous vein harvesting scar) to see what procedures they may have had done and to impress your examiners.
P: If stable angina is present, without history of MI, and with normal resting ECG and normal BP, then annual mortality is about 1.5%
If risk factors are present, then annual mortality greatly increases:
Abnormal ECG – 8.4%
Hypertension – 7.5%
Both – 12%
T2DM – quoted risks (above) – doubled
Investigations that could be used in the work-up of stable angina.
Below is an outline of the investigations that may be used in the work-up of stable angina.
ECG – will often be normal – a normal ECG does not exclude a diagnosis of angina or ACS! If performed during an episode of angina (e.g. during an exercise tolerance test – aka stress test) then typical changes on an ECG might include:
ST-depression
Ventricular ectopic beats
Bundle branch abnormalities – mainly LBBB
CXR
Useful to look for other causes of chest pain (e.g. pneumonia, pneumothorax)
May shown signs of heart failure, which may be associated with severe coronary artery disease
ETT – Exercise tolerance test – aka exersize stress test. Can be ECG or echo after exercise stress.
Assess for symptoms and ECG changes when the heart is stressed
Exercise increases cardiac load and can provoke myocardial ischaemia – which manifests as chest pain, dyspnoea and ECG changes
Has sensitivity of about 90% but a specificity of only about 70%
ECG based ETT should not be used for a diagnosis of stable angina, and is more commonly used after a single acute episode of chest pain to rule out coronary artery disease
Stress echo is a variation of the stress test which can be used to diagnose stable angina (see below)
CTCA
Recommended by NICE is the primary diagnostic investigation
A type of high resolution CT scan, with contrast – injected through a peripheral cannula
A non-invasive test
Typically takes about 10-15 seconds. Scan conducted whilst patient holds their breath
The contrast fills the coronary arteries and can indicate where they are narrowed
Has a very good negative predictive value for cardiovascular disease
Not as sensitive as coronary angiogram – (see below) – whereby the contrast is injected directly into the coronary vessels through a cardiac catheter.
MPS – myocardial perfusion scan
An alternative to CTCA
Is a type of stress test – shows blood flow to different areas of the heart during exercise
Reduced blood flow to any given area can indicate vessel blockage in the vessel associated with that particular area of the heart
Does NOT directly visualise the arteries
It is a nuclear medicine scan – typically using technetium
Results are reported as a “risk stratification” – coronary artery disease, normal, or equivocal
If equivocal – will need other form of imaging to assess if CAD is present
Echocardiograph – may be considered to establish the level of left ventricular function
Can either be performed at rest, or as a stress test
Echo gives information about left ventricular function and ventricular and atrial wall motion defects
Wall motion defects at rest are due to previous MI
On stress test, stress-induced ischaemia may show similar, reversible changes
Stress echo is an echo performed immediately after exercise stress (i.e. within seconds). It can assess for “dynamic” (i.e. they ‘come-and-go’) contraction changes. Particularly useful in stable angina, when a resting echo may be normal, but a stress echo shows changes of ischaemia.
Stress echo provides similar risk stratification to MPS – i.e. it can tell if coronary artery disease is “present” or “absent” but not the location and degree of the abnormality
Pharmacological stress testing can be performed in individuals who cannot exercise. In this instance, medication is given to increase cardiac output – placing similar stresses on the heart as exercise.
Left-ventricular ejection fraction (LVEF) (at rest) is a strong predictor of long-term outcome
LVEF >50% – 12 year survival = 75%
LVEF 35-49% – 12 year survival = 55%
LVEF <35% – 12 year survival = 21%
Angiogram – is the most accurate diagnostic test for coronary artery disease (and therefore for stable angina), But it is relatively expensive, and not without risk, and not necessary for the diagnosis.
An invasive test – requires the insertion of a cardiac catheter
This gives exact information on the level of narrowing of the coronary arteries, and which vessels are affected. It is particularly useful to help determine if revascularisation is necessary. With medical treatment only (without revascularisation), 12-year survival rates are:
Single vessel disease – 75%
Two vessel disease – 59%
Triple vessel disease – 50%
Its main indication is to assess the extent of coronary artery lesions when revascularisation therapies (e.g. stenting (PCI) or bypass) are being considered. As such it is typically reserved for the most symptomatic patients, although its use is increasing.
Coronary artery narrowing is considered significant when the luminal diameter is reduced by >70%
In particular, proximal narrowing of the left main coronary artery and the left anterior descending artery is associated with a poor prognosis.
The preferred test when the patient already has known coronary artery disease and the clinician wants to assess the extent of the disease
Blood tests – for screening of risk factors – cholesterol, fasting glucose
Risk stratification of angina
The presence of angina indicates underlying coronary artery disease. The next step is to evaluate the severity of this underlying cardiac disease, for the purposes of assessing future risk of myocardial infarction – and in particular whether or not revascularisation (e.g. coronary artery stenting, or coronary artery bypass graft – CABG) is indicated. Prognostic indicators include:
Left ventricular function Stress testing (e.g. treadmill or pharmacological stress test) Coronary artery disease extent as seen on angiogram Age Diabetes Hypertension Hypercholesterolaemia Heart failure
Management of stable angina, lifestyle and pharmacological.
This can be divided into lifestyle modifications, pharmacological interventions, and revascularisation.
Lifestyle
Diet advice – plant-based whole foods diet (e.g. mediterranean diet) has been shown to improve long term outcomes
Smoking cessation
After 2 years, risk of MI is same as for those who have never smoked
Control hypertension
Treat hyperlipidaemia – start statin regardless of cholesterol levels
Alcohol – within safe drinking limits
No more than 2 standard drinks on any single day, and two days per week with no alcohol intake
Weight – aim for BMI <=25
Regular exercise – 150 minutes per week of moderate intensity exercise – reduces cardiovascular risk regardless of weight loss, by up to 30%
Pharmacological
There are two main mechanisms used to relieve the symptoms of angina:
Increasing blood flow to the heart muscle (by dilating coronary arteries) – e.g. wth GTN (Glycerytrinitrate)
Decreasing the workload on the heart (e.g. with beta-blocker or calcium channel blocker long term)
First line treatment
Beta-blocker (e.g. atenolol or metoprolol)
Proven to reduce MI and sudden death risk
Decreases heart rate, contractility, and cardiac output – which reduces cardiac O2 demand
e.g. metoprolol 25mg BD
Calcium channel blocker (e.g. verapamil, diltiazem)
These two agents are preferred due to their negative chronotropic events
Typically reserved for patients who are unable to tolerate beta-blockers or whose symptoms are incompletely controlled with beta-blockers
e.g. verapamil 120mg OD
Nitrates
Patients will also likely carry GTN spray or pills with them at all times to relieve acute episodes.
Nitrates cause vasodilation
Can cause hypotension
Provide quick relief – within a couple of minutes, and lasts for up to 30 minutes
e.g. GTN sublingual spray 400mcg – repeat every 5 minutes as required
GTN sublingual tablets 300mcg are also available
Aspirin (or another anti platelet drug – such as clopidogrel or ticagrelor)
Reduced the risk of thrombus formation and thus ACS
e.g. aspirin 100mg daily
Second line treatment
Consider adding…
Long acting nitrate e.g. isosorbide mononitritae 30mg PO OD – up to a max of 120mg daily Typically effect lasts for 4-6 hours Nicorandil Ivabradine Ranolazine Third line treatment
Consider PCI (cardiac stent, balloon angioplasty)
Typically both balloon angioplasty and stenting are performed simultaneously
The procedure carries a 1-3% mortality, and 5% risk of MI
There is no evidence that angioplasty (+/- stent) improves survival or reduces risk of ACS. It may however reduce symptoms of stable angina
CABG – Coronary arty bypass graft
Similar risks as PCI (above)
Completely eliminates symptoms in about 85% of patients
Does not appear to improve survival for those with class I or II disease (see above)
Modest improvement in survival for those with left main coronary artery disease or triple vessel disease
Patients with T2DM have better outcomes with CABG than PCI
Cardiorespiratory arrest
D: Cardiac arrest is an ‘arrest’ in the activity of the heart – the heart has stopped beating. There will be no contraction of the heart muscle, but there may still be electrical activity in the heart (we call this PEA = pulse-less electrical activity).
Irreversible brain damage can occur after <5 minutes of cardiac arrest. When you carry out CPR, you are trying to reverse the affects of cardiac arrest by proving a cardiac output – at first manually with chest compression, and hopefully later with ROSC – Return of Spontaneous Circulation – when the heart starts beating again.
R:
D:
E:
A: In some cases, cardiac arrest may be reversible. The causes of reversible cardiac arrest are the 5H’s and the 4T’s. H's: -Hypoxia -Hypovolaemia -Hypokalaemia -Hyperka;aemia -Hypothermia. T's: -Tension pneumothorax -Tamponade (cardiac) -Toxins -Thrombosis.
M:
Defibrillation and cardioversion
When you pass a large current through the heart, you can completely depolarise it. After this time, there will be a period of asystole, hopefully after which normal sinus mechanisms will restore sinus rhythm to the heart.
Defibrillators deliver a high-voltage, short duration DC shock, via two metal pads (coated in conducting gel or jelly) placed on the chest.
These should be placed over the upper right sternal edge and the apex.
You can also deliver a shock right to the heart during open surgery!
Defibrillation vs cardioversion – defibrillation is a general term often used to describe the shock given to the heart, and more specifically it describes an ‘unsynchronised ‘shock. Cardioversion refers to this shock when it is applied at a specific time in the ECG cycle (a ‘synchronised’ shock).
Before attempting to shock the heart, you need to establish what the current rhythm is. Determining the rhythm determines further treatment options. All this will also take place in the context of CPR.
Beware! – if you give a shock at around the peak of the T wave, you can induce unusual and dangerous rhythms such as atrial fibrillation or ventricular tachycardia. Thus the current is usually synchronised with the ECG so that the pulse is given about 0.02s after the peak of the R wave.
In ventricular fibrillation, the timing of the impulse is not important.
Shockable rhythms:
- Ventricular fibrillation
- Pulseless ventricular tachycardia.
Non-shockable rhythms:
PEA – pulseless electrical activity – this means any electrical activity that appears on an ECG like it should be producing a pulse, but it is not. The most common cause is hypovolaemia.
Asystole – no rhythm present
Cardioversion therapy is often pre-planned, and used to treat significant, although not immediately life-threatening arrhythmias, such as narrow complex tachycardias, atrial fibrillation and atrial flutter.
Sedation or no sedation?
in an emergency situation, the patient is often unconscious as a result of cardiogenic shock, and in such cases, there is no anaesthesia given. In cases where the patient is awake (most commonly elective cardioversion), then the patient may receive sedation to make the treatment more tolerable.
Contraindications and complications
Digoxin – this increases the risk of arrhythmias after cardioversion, and thus in cases of elective cardioversion, the drug is usually withheld for 24 hours before treatment.
Risk of systemic embolus – is increased in patients with long standing atrial arrhythmias who undergo elective cardioversion. Thus, these patients should be given 4 weeks anticoagulant therapy for at least 4 weeks either side of the treatment.
P: Cardiac arrest is a medical emergency, and has extremely poor prognosis.
Out of hospital arrest has a survival rate of 2-8%
In hospital cardiac arrest has a 1-year survival rate of about 15%. The best centres in the world have a ‘survival to discharge’ of up to 50%
Prognosis is particularly dependent on the electrical rhythm of the heart during the arrest.
Which layers of the aorta are affected in aortic dissection?
Tear in tunica intima. The tear only occurs in the tunica intima and this causes a separation of the tunica intima and tunica media layers.
Which diuretics acts on the sodium-chloride transporter of the distal tubule?
Bendroflumethiazide - inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule
What is a common side effect of amlodipine?
Ankle swelling is a common side-effect of amlodipine. According to NICE guidelines thiazide diuretics can be used instead of calcium channel blockers in the initial management of hypertension in patients over 55.
Mannitol is an osmotic diuretic that is used to lower intracranial pressure following a head injury. Spironolactone is an aldosterone antagonist. Furosemide acts on the thick ascending loop of Henle to prevent reabsorption of potassium, sodium, and chloride. Acetazolamide is a carbonic anhydrase inhibitor that is used to treat acute angle closure glaucoma.
What is the mechanism of action of bosentan?
Bosentan - endothelin-1 receptor antagonist
A 29-year-old male with ankylosing spondylitis is examined by his GP. On palpation of the carotid pulse, the GP notes a pulse that rapidly rises and then falls and upon auscultation of the heart hears a high-pitched early diastolic murmur, which is decrescendo in nature. Which cardiac abnormality do these examination findings suggest?
Aortic regurgitation.
Aortic regurgitation typically causes an early diastolic murmur
The murmur heard in aortic regurgitation occurs early in diastole due to the backflow of blood from the aorta into the left ventricle through an incompetent aortic valve.
The carotid pulse rises rapidly due to the vigorous ejection of blood from an overloaded left ventricle. It then falls rapidly due to the backflow of blood into the left ventricle.
Patients with aortic regurgitation may also have an ejection murmur, caused by the turbulent ejection of blood from the overloaded left ventricle.
Aortic regurgitation due to aortic root dilation can be associated with ankylosing spondylitis, Marfan syndrome or aortic dissection. Causes of aortic regurgitation due to aortic valve leaflet disease are calcific degeneration, congenital bicuspid aortic valve, rheumatic heart disease and infective endocarditis.
During surgery on his neck, a man suffers a vagus nerve injury where the nerve is cut near the exit from the skull. He wakes up with a high heart rate and high blood pressure due to loss of parasympathetic tone.
Which of the following other features would be expected with a vagus nerve injury?
Pupillary constriction Loss of anal tone Erectile dysfunction Urinary retention Hoarse voice
Hoarse voice.
All innervation for speech originates from the vagus (X) nerve so injuries to the vagus will cause speech problems.
Remember that the vagus nerve has both autonomic and somatic effects; the most important somatic pathway being motor supply to the larynx via the recurrent laryngeal nerves, which are branches of the vagus. Damage to one vagus nerve would therefore result in the same effect as damage to a single recurrent laryngeal which is a hoarse voice.
Anal tone, erections and urination are all controlled by the sacral parasympathetics and would not be affected by loss of the vagus. Pupillary constriction is controlled by parasympathetics on the oculomotor nerve and so would also not be affected by loss of the vagus.
Angina pectoris
Angina pectoris may be defined as:
Signs and Symptoms:
An acute pain in the thorax lasting seconds to minutes (according to WHO < 20 min).
Typically, the pain radiates out into the left shoulder/arm or neck region.
May be a vague, barely troublesome ache, or it may rapidly become a severe, intense precordial crushing sensation.
Aetiology:
The cause is usually critical coronary artery obstruction due to atherosclerosis.
Pathogenesis:
Angina pectoris occurs when the myocardial oxygen demand exceeds the ability of the coronary arteries to supply oxygenated blood.
Treatment:
Glyceyl nitrate is a potent smooth-muscle relaxer and vasodilator. It lowers systolic BP and dilates systemic veins, thus reducing myocardial wall tension, a major determinant of oxygen demand.
Beta-blockers block sympathetic stimulation of the heart and reduce systolic pressure, heart rate, contractility, and cardiac output, thus decreasing myocardial oxygen demand and increasing excercise tolerance.
Calcium channel blockers are vasodilators useful in the treatment of angina with hypertension. They are also used in the treatment of variant or Prinzmetal’s angina where they prevent coronary artery spasm.
Usually non dihydropiridin derived calcium antagonists are used when beta-blockers are contraindicated or not clinically effective.
ST elevation
The ST elevation can be clearly seen on the ECG; this is common in the early stages of a heart attack. Since these changes are observed in leads II, III, AVL, AVF, and V4-6 he has an inferolateral STEMI.
A diagnosis of MI is confirmed by 2 out of 3 of the following findings:
Clinical picture (typical chest pain)
Appropriate laboratory evidence showing elevated enzymes (troponin, CK,)
ECG changes
So now that you are quite certain of the diagnosis, how would you treat Mr.
Lignocaine
Lignocaine is only necessary if the patient developes a ventricular arrythmia. This is a common complication within the first 24 hours.
Benzodiazepine
If the patient is very anxious, benzodiazepines may improve this problem and indirectly lower the heart rate. However, the patient must not be given intramuscular injections (any medication) as this will make a treatment with plasminogen activators impossible!
If benzodiazepines are essential, they should be given orally or iv.
Treaatment fot acute MI
sTATIN
Heparin: This could be given iv (unfractionated heparin) or sc (low molecular weight heparin).
LMWH is usually given as it is easier and does not require monitoring. It should not be given to patients with renal impairment or those at high risk of bleeding (as it cannot easily be reversed).
This will ease the patient’s pain and reduce his anxiety.
Also B-blocker, indication: bradycardia.
aspirin also needed for treatment
Angiography and angioplasty
?
What are the indications of thrombolysis?
ST elevation 1.5mm in leads II and III–> Acute onset of at least 1mm ST elevation in 2 adjacent limb leads or at least 1mm ST elevation in 2 adjacent precordial leads.
New Left Bundle Branch Block
Symptoms began less than 12 hours ago
ST depression
ST depression generally means that there is an area of ischaemia in the cardiac muscle and therefore this indicates that thrombolysis will not definitely reverse this.
Which of the following options are absolute contraindication to thrombolysis?
Active internal bleeding
Aortic dissection
Previous history of a hemorrhagic stroke
Ischaemic stroke 3 months ago–> relative contraindications, not absolute.
The age of a patient is a relative contraindication, as older patients tend to have a higher risk of developing bleeding complications. One must weigh the risks of thrombolysis on a case by case basis.
Absolute vs relative contraindications of thrombolysis
Absolute contraindications:
Aortic dissection Acute pericarditis Active bleeding Cerebral haemorrhage or known intracerebral vascular disease Relative contraindications:
GI or GU haemorrhage within past 6 months
Stroke within past 6 months
Major surgery
Organ biopsy
Non-compressible vessel puncture within past 2-4 weeks
Prolonged CPR with chest trauma or remaining unconscious
Diabetic proliferative retinopathy
Severe uncontrolled hypertension (SBP>200 or DBP>120)
History of bleeding diathesis or hepatic dysfunction or cancer
Pregnancy
What are the indications for Angiography and Angioplasty?
Pain started less than 12 hours ago.
Angioplasty can take place within first 90 mins after symptoms onset
An Interventional cardiologist should be available to perform the procedure.
He should also be linked to an experienced department with a coronary care unit.
Risks of angiography and angioplasty
1 in 100 risk of complete occlusion of coronary artery
1 in 200 risk of damage to coronary artery, both which may require an emergency CABG
Puncture site haematoma, infection or false aneurysm.
Internal bleeding as a result of the anticoagulation therap
(Possible, but unlikely. In a hypovolemic shock, the patient would have cold peripheries, but also a low CVP.)
Complication of angioplasty:
Early reocclusion and proagation of the infarction area. Pericardial tamponade (this is possible and is a recognised complication of angioplasty. The absence of pulsus paradox makes it less likely.) -Right ventricular infarct: This could well be the case since he is quite breathless
Echocardiography
This will be useful in excluding pericardial tamponade. It will also assess LV and RV function and look for regional wall abnormalities
ECG
to assess myocardial infarction.
To diagnose extension of myocardial ischemia, an ECG with additional right-ventricular leads (V1R-V6R) would be helpful.
An ECG would also help to determine if there is regional damage in the contraction of the right or left ventricle and also give an indication of the presence of a pericardial effusion (low ECG voltage).
Septic shock diagnostic factors
CVP normal/low
Patient is warm (hyperdynamic form)
Anaphylactic shock
The most important disgnostic factors in this instance are:
CVP low
Patient is warm
History
cardiogenic shock
The most important diagnostic factors in this instance are:
CVP mostly high
Patient is cold.
Treated with dobutamine
hypovolaemic shock
The most important disgnostic factors in this instance are:
Low CVP
Patient is cold
DOPAMINE
Dopamine is an intermediate in tyrosine metabloism and precursor of norepinephrine and epinephrine; it accounts for 90% of the catecholamines. Dopamine affects dopamine receptors at low doses and raises the perfusion in the splanchnic and renal areas. At intermediate levels, dopamine works on beta-receptors causing a positive inotropic effect with minimal peripheral vasoconstriction. At high doses, dopamine works on alpha-receptors and causes distinct peripheral vasoconstriction. Since there is a clear elevation of the afterload, dopamine appears to have a negative effect on the heart.
dobutamine
Dobutamine is a synthetic derivative of dopamine. It is a direct acting inotropic agent which causes stimulation of the beta receptors of the heart while producing less marked chronotropic, hypertensive, arrhythmogenic or vasodilatory effects. It does not cause the release of endogenous noradrenaline as does dopamine and it has no specific effect on the renal vasculature. In both animal and human studies, dobutamine produces a reduced increase in heart rate and a reduced decrease in peripheral vascular resistance for a given inotropic effect than does isoproterenol.
VTE Prevention prophylaxis
- Mechanical methods (graduated compression stockings and intermittent pneumatic compression devices)
- Pharmacological agents
- Conservative: early mobilisation, stay hydrated.
NSTEMI
NSTEMI is usually diagnosed on the basis of:
A suggestive history
Elevated troponin levels
Be aware that any condition that causes myocardial damage can result in an elevated troponin. Examples of other causes of elevated troponin include PE, myocarditis, renal failure (chronically raised).
What is particularly important is the pattern of the troponin result (see below)
ECG changes
An absence of ST evevation
ECG may be normal
There may be other changes on ECG to suggest MI. These might include:
ST depression
Hyperacute T wave (tall pointy T waves) – often an early sign which resolve but the time the patient is seen in hospital
TWI (T-wave inversion) – a late sign, often indicates previous MI
Non-specific ST changes
Unstable angina
Unstable angina is distinguishable from NSTEMI only through troponin results.
Troponin – negative
ECG changes – as for NSTEMI above
Dressler’s Syndrome
Dressler’s Syndrome
This is also called post-myocardial infarction syndrome. It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart). It is less common as the management of ACS becomes more advanced.
It presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation. It can cause a pericardial effusion 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), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).
Management is with NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis to remove fluid from around the heart.
prevention of MI
Secondary Prevention Medical Management (6 As)
Aspirin 75mg once daily
Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
Atenolol (or other beta blocker titrated as high as tolerated)
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted. This is due to a higher risk of thrombus formation in different stents.
Secondary Prevention Lifestyle:
Stop smoking
Reduce alcohol consumption
Mediterranean diet
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions (e.g. diabetes and hypertension)
Atherosclerosis
Atherosclerosis is a chronic inflammatory process affecEng the in&ma of arteries. It is
characterised by the formaEon of lipid-rich plaques in the vessel wall.
Atherosclerosis pathophysiology
For pracEcal purposes the inEma equates to the endothelium (the layer of cells that lines the interior
surface of the circulatory system).
The important *modifiable risk factors for developing atherosclerosis are:
• smoking
• hypertension
• diabetes mellitus
• dyslipidaemia (abnormal lipoprotein levels ie. high raEo of LDL:HDL)
All four of these risk factors damage the endothelium.
The damaged endothelial cells become dysfunc&onal:
• there is increased permeability.
• they produce adhesion molecules and cytokines which
aSract inflammatory cells and prothromboEc molecules.
eg. VCAM-1 (vascular cell adhesion molecule-1) binds
monocytes and T cells.
Consequently, there is recruitment of inflammatory cells to
the site of injury: monocytes and T cells adhere to the
endothelium and migrate into the inEma. The monocytes
differenEate into macrophages.
The macrophages have a number of effects:
• they produce free radicals that drive LDL oxidaEon to
form oxidised LDL.
[Remember: naEve LDL is not atherogenic.
oxidised LDL is highly atherogenic.]
• they engulf oxidised LDL and cholesterol crystals,
becoming foam cells.
[A foam cell is a macrophage containing abundant
lipid in its cytoplasm, giving the cytoplasm a ‘foamy’
appearance microscopically - hence the name].
• foam cells produce growth factors what sEmulate
migraEon of smooth muscle cells from the media to the
inEma.
The migraEon and acEvaEon of smooth muscle cells is also
driven by factors released by acEvated platelets and
endothelial cells.
*Do not forget the most important non-modifiable risk factors for developing atherosclerosis:
family history and male gender.
Other modifiable risk factors include obesity, diet and exercise.
Endothelial Injury
Atherosclerosis is a chronic inflammatory process affecEng the in&ma of arteries. It is
characterised by the formaEon of lipid-rich plaques in the vessel wall.
turn over
Fatty streak
Oxidised LDL accumulates within macrophages and
smooth muscle cells just underneath the endothelial cells.
CollecEons of lipid-laden macrophages siyng in the
inEmal layer may be visible as yellow elevaEons called
faSy streaks. The faSy streak has no clinical significance
but it is important because it may progress to an
atheroscleroEc plaque.
Atherosclerotic plaque
A core of lipid debris forms as the foamy macrophages die
and the lipid in their cytoplasm is released.
Smooth muscle cells proliferate and change their
behaviour: they secrete collagen and other extracellular
matrix proteins (rather than being contracEle), resulEng in
the formaEon of a fibrous cap over the core. The core is
composed of oxidised lipid and inflammatory cells.
The cap represents the body’s aSempt to repair by
scarring (see InflammaEon lecture notes pg 5).
Atherosclerosis exhibits the three hallmarks of a chronic inflammatory process
- persistent injury (endothelial damage due to the previously described risk factors).
- on-going inflammaEon (macrophages and lymphocytes).
- repair with scarring (the fibrous cap of the plaque).
Shockable vs non shockable cardiac arrest rhythms
Four Cardiac Arrest Rhythms
These are the four possible rhythms that you will see in a pulseless unresponsive patient. They can be categorised into shockable (meaning defibrillation may be effective) and non-shockable (meaning defibrillation will not be effective and should not be used).
Shockable rhythms:
Ventricular tachycardia
Ventricular fibrillation
Non-shockable rhythms:
Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
Asystole (no significant electrical activity)
Supraventricular tachycardias
Supraventricular tachycardia (SVT) is caused by the electrical signal re-entering the atria from the ventricles. Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12). It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.
Paroxysmal SVT describes a situation where SVT reoccurs and remits in the same patient over time.
There are three main types of SVT based on the source of the electrical signal:
“Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node.
“Atrioventricular re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome).
“Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. This ectopic electrical activity causes an atrial rate of >100bpm.
Acute Management of Stable patients with SVT
When managing SVT take a stepwise approach trying each step to see whether it works before moving on. Make sure they are on continuous ECG monitoring.
Valsalva manoeuvre. Ask the patient to blow hard against resistance, for example into a plastic syringe.
Carotid sinus massage. Massage the carotid on one side gently with two fingers.
Adenosine (see below)
An alternative to adenosine is verapamil (calcium channel blocker)
Direct current cardioversion may be required if the above treatment fails
Adenosine
Adenosine works by slowing cardiac conduction primarily though the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway. It will often cause a brief period of asystole or bradycardia that can be scary for the patient and doctor, however it is quickly metabolised and sinus rhythm should return.
A few key points on administering adenosine:
Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension
Warn patient about the scary feeling of dying / impending doom when injected
Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa)
Initially 6mg, then 12mg and further 12mg if no improvement between doses
Long Term Management of patients with paroxysmal SVT
When patients develops recurrent episodes of SVT then measures can be taken to prevent these episodes. The options are:
Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation
Wolff-Parkinson White Syndrome
Wolff-Parkinson White Syndrome is caused by an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent.
The definitive treatment for Wolff-Parkinson White syndrome is radiofrequency ablation of the accessory pathway.
ECG Changes:
Short PR interval (< 0.12 seconds)
Wide QRS complex (> 0.12 seconds)
“Delta wave” which is a slurred upstroke on the QRS complex
Note: If the person has a combination of atrial fibrillation or atrial flutter and WPW there is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia. Most antiarrhythmic medications (beta blockers, calcium channel blockers, adenosine etc) increase the risk of this by reducing conduction through the AV node and therefore promoting conduction through the accessory pathway – therefore they are contraindicated in patients with WPW that develop atrial fibrillation or flutter.
Radiofrequency ablation
Radiofrequency Ablation (RFA) Catheter ablation is performed in a electrophysiology laboratory, often called a “cath lab”. It involves local or general anaesthetic, inserting a catheter in to the femoral veins and feeding a wire through the venous system under xray guidance to the heart. Once in the heart it is placed against different areas to test the electrical signals at that point. This way the operator can hopefully find the location of any abnormal electrical pathways. The operator may try to induce the arrhythmia to make the abnormal pathways easier to find. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity. The aim is to remove the source of the arrhythmia.
This can be curative for certain cases of arrhythmia caused by abnormal electrical pathways, including:
Atrial Fibrillation
Atrial Flutter
Supraventricular Tachycardias
Wolff-Parkinson-White Syndrome
Ventricular Ectopics
Ventricular ectopics are premature ventricular beats caused by random electrical discharges from outside the atria. Patients often present complaining of random, brief palpitations (“an abnormal beat”). They are relatively common at all ages and in healthy patients however they are more common in patients with pre-existing heart conditions (e.g. ischaemic heart disease or heart failure).
They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG.
Bigeminy
This is where the ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on.
Management
Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
Reassurance and no treatment in otherwise healthy people
Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)
Torsades de pointes
Torsades de pointes is a type of polymorphic (multiple shape) ventricular tachycardia. It translates from French as “twisting of the tips”, describing the ECG characteristics. It looks like normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes progressively get smaller, then larger then smaller and so on. It occurs in patients with a prolonged QT interval.
A prolonged QT interval is the ECG finding of prolonged repolarisation of the muscle cells in the heart after a contraction. Depolarisation is the electrical process that leads to the heart contraction. Repolarisation is a period of recovery before the heart muscle cells (myocytes) are ready to depolarise again. Waiting a longer time for repolarisation can result in random spontaneous depolarisation in some areas of heart myocytes. These abnormal spontaneous depolarisations prior to repolarisation are known as “afterdepolarisations”. These depolarisations spread throughout the ventricle, leading to a ventricular contraction prior to proper repolarisation occurring. When this occurs and the ventricles continue to stimulate recurrent contractions without normal repolarisation it is called Torsades de pointes.
When a patient develops Torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress in to ventricular tachycardia. Usually they are self limiting but if they progress to VT it can lead to a cardiac arrest.
Causes of Prolonged QT
Long QT Syndrome (inherited)
Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
Acute Management of Torsades de pointes
Correct the cause (electrolyte disturbances or medications)
Magnesium infusion (even if they have a normal serum magnesium)
Defibrillation if VT occurs
Long Term Management of Prolonged QT Syndrome
Avoid medications that prolong the QT interval Correct electrolyte disturbances Beta blockers (not sotalol) Pacemaker or implantable defibrillator
What 3 things on ECG for NSTEMI
- ST segment depression.
- Deep T wave inversion.
- Pathological Q waves: suggests a deep infarct and is a late sign.
What things on ECG for stemi
- Look for ST elevation greater than or equal to 0.2 millimeters and leads v1 to v3 or greater than or equal to 0.1mm, which is a small square on the ECG charts in any other leads.
- left bundle branch block.
If someone comes in with new LBBB, and they have a convincing history of MI, that convinces you that they are having a STEMI.
management of a&e ST elevation MI
A number of studies over the past 10 years have provided an evidence for the management of ST-elevation myocardial infarction (STEMI)
In the absence of contraindications, all patients should be given
aspirin
P2Y12-receptor antagonist. Clopidogrel was the first P2Y12-receptor antagonist to be widely used but now ticagrelor is often favoured as studies have shown improved outcomes compared to clopidogrel, but at the expense of slightly higher rates of bleeding. This approached is supported in SIGN’s 2016 guidelines. They also recommend that prasugrel (another P2Y12-receptor antagonist) could be considered if the patient is going to have a percutaneous coronary intervention
unfractionated heparin is usually given for patients who’re are going to have a PCI. Alternatives include low-molecular weight heparin
NICE suggest the following in terms of oxygen therapy:
do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:
people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%
people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.
Primary percutaneous coronary intervention (PCI) has emerged as the gold-standard treatment for STEMI but is not available in all centres. Thrombolysis should be performed in patients without access to primary PCI
With regards to thrombolysis:
tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase
tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile
A 65-year-old gentlemen presents to the General Practitioner (GP) with shortness of breath, fatigue, and a malar flush on his cheeks. Cardiovascular examination reveals a regular, low-volume pulse and a mid-diastolic murmur loudest with the patient leaning to his left-hand side. What does patient have?
This patient has severe, symptomatic mitral stenosis.
P Mitrale represents left atrial hypertrophy/strain e.g. in mitral stenosis
The bifid P wave is termed P Mitrale since mitral valve stenosis is the commonest cause of its appearance on EC
Examples of when you would see the following on ecg rbbb p mitrale p pulmonale tented t waves LBBB
The bifid P wave is termed P Mitrale since mitral valve stenosis is the commonest cause of its appearance on ECG. Right bundle branch block is often a sign of problems on the right side of the heart such as right ventricular hypertrophy, cor pulmonale, pulmonary embolism, and is not a common ECG finding in mitral stenosis. Left bundle branch block is also not a common finding in mitral stenosis, with common causes including ischaemic heart disease, hypertension, aortic stenosis, and cardiomyopathy. Tall Tented T waves are seen in hyperkalaemia, and P Pulmonale (which looks like a peaked P wave) reflects any process causing the right atrium to become hypertrophied such as tricuspid regurgitation and pulmonary hypertension.
