Cardio Topic List Flashcards
Definition and diagnosis of hypertension.
Aortic stenosis.
Aortic stenosis
• Aortic valve stenosis (AS) is a valvular heart disease characterized by narrowing of the aortic valve.
Normally, the orifice is about 4cm2 but in the case of severe AS it may reduce to under 1cm2
. As a result, the outflow of blood from the left ventricle into the aorta is obstructed.
• This leads to chronic and progressive excess load on the left ventricle and potentially left ventricular failure.
The patient may remain asymptomatic for long periods of time; for this reason, AS is often detected late when it first becomes symptomatic (Syncope, angina pectoris, or dyspnea upon • • • • • exertion).
Auscultation reveals a harsh, crescendo-decrescendo murmur in systole that radiates to the carotids, and pulses are delayed with diminished carotid upstrokes.
Echocardiography is the noninvasive gold standard for diagnosis. Patients with mild asymptomatic aortic stenosis are treated conservatively with monitoring and medical management of related conditions (e.g. hypertension).
Symptomatic patients, or those with severe aortic valve stenosis, require immediate aortic valve replacement (AVR) as definitive treatment.
Options for valve replacement include surgical AVR or transcatheter AVR (TAVR) for patients with high operative risk. Patients with severe AS have a high risk of developing acute complications such as heart failure and cardiogenic shock, which are challenging to manage and often require critical care interventions and expedited surgery or TAVR.
- Epidemiology – aortic stenosis is the most common valvular heart disease in industrialized countries and is frequently associated with aortic regurgitation (topic 14)
- Etiology
a. Aortic valve sclerosis – calcification and fibrosis of the leaflets (wear and tear)
i. This is the most common cause of aortic stenosisb. c. d.
ii. Prevalence increases with age (35% in patients over 80 years old)
Bicuspid aortic valve – fusion of two leaflets in uteroi. Having two leaflets predisposes the aortic valve to dystrophic calcificationRheumatic fever (typically affects the mitral valve) but may predispose ASEndocarditis (least common cause)
- Pathophysiology: Narrowed opening area of the aortic valve during systole → obstruction of blood flow from left ventricle (LV) → increased LV pressure → left ventricular concentric hypertrophy, which leads to:
a. b. Impaired ventricular filling during diastole → left heart failure
- Clinical features – usually remains asymptomatic for years but may show symptoms in severe stenosis.
a. Signs and symptoms (also indications for valve replacement): SAD (3 major Sx)
i. Syncope
ii. Angina pectoris
b.
iii. Dyspnea
iv. Fatigue Physical exam
i. Small BP amplitude, decreased pulse pressure (normal is between 30-40 mmHg)
ii. Weak and delayed distal pulse (“pulsus parvus et tardus”)
c. Auscultation
i. Harsh crescendo-decrescendo systolic murmur which is best heard in the 2nd right IC
ii. space (may also be heard in the carotids) Severe AS is characterized by a soft S25 sound
iii. An early systolic ejection click may also be heard
- Diagnosis
a. Echocardiography – the preferred method for diagnosing AS; LV function, LV wall thickness, aortic valve area, transvalvular systolic gradient and LA dimensions should be measured.
i. Transthoracic echo is the primary test as it is noninvasive.
Transesophageal echo is a second-line modality used for confirmation of TTE
ii. 6. 7. findings.
Medical therapy
a. No medical therapy can improve outcome
b. Coexisting HTN should be treated
c. Ensure maintenance of sinus rhythmIndications for intervention
a. b. c. Intervention is indicated in symptomatic patients with severe, high-gradient aortic stenosis (mean gradient ≥40mmHg), and in asymptomatic patients with severe AS and lowered LVEF (<50%).
Surgical aortic valve replacement is recommended in patients with low surgical risk.
Transcatheter aortic valve replacement (TAVR) is recommended in patients who are not suitable for surgery
- Treatmenta. TAVR – recommended for patients with high surgical risk and predicted survival of > 12 months. Can be down transfemoral, transaortic, or transapical (pierce the heart).
Procedure: https://www.youtube.com/watch?v=ldvchT0LHF0i.
ii. Valve options: https://www.youtube.com/watch?v=92fjJzxKRPo
b. Percutaneous balloon valvuloplasty
6 – used in younger patients who do not have any AV calcification.
Ischemic heart disease (risk factors, manifestations, diagnosis).
Rehabilitation in cardiology.
(Check Table in note)
Rehabilitation in cardiology
Cardiac rehabilitation is a comprehensive exercise, education, and behavior modification programwith a goal of helping patients restore and maintain optimal health while helping to reduce the risk of future heart problems. It is a professionally supervised program which aims to help patients recover from MI, surgery and other cardiac procedures.
The first stages of most cardiac rehabilitation programs generally last about three months, but some people will follow the program for longer.
In special situations, some people might be able to do an intensive program for several hours a day that can last only one or two weeks.
During the rehabilitation process, patients will work with a team which consists of cardiologists, nurses, dietitians, physical therapists, and mental health specialists.
The rehabilitation includes a medical evaluation, physical activity, lifestyle education and other additional support. Depending on the original reason for initiation of therapy, rehabilitation may be either done as an inpatient program or an outpatient program.
Therapies include: nutritional therapies, weight loss programs, management of lipid abnormalities with diet and medication, blood pressure control, diabetes management, stress management, smoking cessation.
Exercise based programs to improve cardiac fitness, microvascular circulation, quality of life and readmission rates.
Mor:Cardiac rehabilitation (cardiac rehab) is a professionally supervised program to help people recover from heart attacks, heart surgery, and percutaneous coronary intervention (PCI) procedures such as stenting and angioplasty.
• Cardiac rehab programs usually provide education and counseling services to help heart patients increase physical fitness, reduce cardiac symptoms, improve health, and reduce the risk of future heart problems, including heart attack.
• Programs often include:
o A medical evaluation to figure out needs and limitations of the patient.
The medical staff uses this information to fit a rehabilitation program for the patient and help set goals.
o A physical activity program according to the patient needs. Heart rate and blood pressure are monitored during physical activity.
o Counseling and education to help the patient understand his/her condition and how to manage it.
The patient may work with a dietitian to create a healthy eating plan.
Counseling on how to stop smoking.
o Support and training to help the patient return to work and normal activities and to help learn to manage his/her heart condition.
Heart failure (common causes, pathophysiology, clinical manifestations, stages).
Diagnosis and treatment of secondary hypertension.
Also check table in note
- S3 and S4 gallop on auscultation
- Crackles/rales at lung base5.
- Dullness on percussion
b. Right sided HF
i. Peripheral pitting edema, nocturia, jugular vein distention (visible swelling of jugular veins due to increased CVP and venous congestion), Kussmaul sign (distension of jugular veins during inspiration due to increased JVP) , hepatomegaly, ascitesStages – New York Heart Association (NYHA) Classificationa.
b. c. Class I – symptoms only occur with vigorous activities.
Patients are nearly asymptomatic
Class II – symptoms occur with prolonged or moderate exertion (stairs or heavy lifting).
Slight limitation of activities. Patients are comfortable at rest.
Class III – symptoms occur with usual activities of daily living (in-house walking, getting dressed). Marked limitations in activity. Comfortable only at rest.
d. Class IV – symptoms occur at rest.
Incapacitating
- Diagnosisa. Transthoracic echocardiogram is the gold standard for evaluating patients with heart
b. c. failure. Assess systolic function (left ventricular ejection fraction) and the diastolic function (diastolic filling and ventricle dilation).
Chest x-ray: signs of cardiomegaly
(boot-shaped heart on PA view) and pulmonary congestion
Lab: Elevated BNP and NT-pro BNP as well as atrial natriuretic peptide (ANP)
Diagnosis and treatment of secondary hypertension
Secondary HTN is HTN which is caused by an identifiable underlying condition. This accounts for 5-15% of cases in adults and 70-85% of cases in children (<12).
Age of onset is usually under 25 or over 55. 1. Causes of secondary HTN a. Can be remembered by the pneumonic RECENT: R – renal, E – endocrine, C – coarctation of aorta, E – estrogen (oral contraceptives), N – neurologic, T – treatment.b. Renal HTN may be caused by:
i. renal artery stenosis, SLE, tumors, ADPKD and renal failurec. Endocrine HTN may be caused by Cushing syndrome, Conn syndrome, hyperthyroidism and
d. e. others.Neurologic can be increased ICP Treatment would refer to the use of NSAIDS, sympathomimetic drugs and corticosteroids.
2. Diagnosis of secondary HTN is a bit more complicated than that of primary HTN.
a. General indicators: young patient, abrupt onset, end-organ damage that is disproportionate to the degree of HTN, recurrent hypertensive crises and resistant HTN8
b. Specific indicators are those which point to the underlying disease therefore urinalysis, complete blood count, blood chemistry profile, and various imaging modalities (ultrasound of kidney and its vessels) may be used to determine the cause.
- Treatment of secondary hypertension is done by treatment of the underlying cause. The underlying conditions are usually treated with medication or surgery if needed (in case of tumors for example). Once the underlying condition is controlled, the HTN usually goes back to normal. If the HTN remains elevated, treatment consists of both pharmacological and nonpharmacological measures (see Topic 14).
Stable angina pectoris, vasospastic angina (diagnosis and treatment).
Pulmonary hypertension.
f. Pulmonary function tests, Arterial blood gases, CT imaging, Cardiac MRITreatment – initial therapy should be directed at the underlying cause.
a. Treatment of the underlying disease in secondary PH.
Supplemental oxygen, diuretics, anticoagulation, digoxin and exercise should be considered in all groupsb.
Group 1 patients (primary PHTN)
i. Bosentan (endothelin-A receptor antagonist, oral, causes vasodilation)
ii. Sildenafil, tadalafil (phosphodiesterase type 5 inhibitor, increases cGMP àpulmonary artery relaxation)
iii. Prostacyclin analogues and prostacyclin receptor antagonist
- Epoprostenol: given IV
c. Group 4 (thromboembolic disease): surgical thrombectomy; anticoagulation and thrombolytics are alternatives for those who cannot undergo surgery
Acute coronary syndrome (unstable angina, NSTEMI, STEMI): diagnosis, algorithms of the
treatment.
Myocarditis and rheumatic fever.
(Check table in note)
b. c. d. e. f. Pharmacological inhibition of platelet aggregation and anti-coagulation (Na+ heparin)Coronary revascularization as soon as possible (usually percutaneous)
Continuous monitoring (rhythm, hemodynamics, blood gas parameters, etc.)
Treatment of complications
Follow the chart below
i. NOTE: STEMI – primary PCI if possible, fibrinolysis only when primary PCI is delayed (more than 120 minutes)or not possible, and facilitated or rescue-PCI has to be performed, if necessary.
ii. For primary PCI (both in STEMI and NSTEMI), the recommended procedural access is the radial artery.
Treatment consists in opening and dilation of the vessels responsible for infarction and implantation of drug-eluting stent
Myocarditis and rheumatic fever
Myocarditis is an inflammatory disease of the myocardium that most often affects young patients, causing approx. 10% of sudden deaths in young adults.
The disease is commonly caused by viral infections or acute rheumatic fever, but may also manifest in patients with systemic conditions such as systemic lupus erythematosus or vasculitic syndromes.
Adult patients are commonly asymptomatic or present with nonspecific symptoms, including fever, fatigue, and weakness. Some patients also experience cardiac signs that vary in severity from chest pain and arrhythmias to heart failure or sudden cardiac death.
Infants and children typically have a more severe presentation. Inflammation may also spread and lead to concurrent pericarditis.
Myocarditis should be suspected in patients with a history of flulike symptoms and new evidence of ECG abnormalities, such as sinus tachycardia or concave ST-segment elevations.
Further diagnostic tests may show elevated cardiac enzymes and cardiac enlargement in chest x-rays.
If the diagnosis is uncertain, an additional myocardial biopsy may also be indicated.
Initial management of myocarditis involves supportive measures and treatment of any underlying diseases (e.g., antibiotic therapy).
Cardiac symptoms usually require additional medication, including amiodarone for arrhythmias or β-blockers for congestive heart failure.
Whereas most adults with viral myocarditis make a full recovery, there is a small risk of the condition progressing to dilated cardiomyopathy.
The prognosis is especially poor for infants and small children.
- Etiologya. Infectious
i. Viral: Coxsackie A and B, echovirus, parvovirus B-19, varicella, HCV, HIV, EBV, CMV
ii. Bacterial: Group A strep, C. diphtheriae, B. burgdorferi, mycobacterium, pneumococci, haemophilus
iii. Fungal: candida, aspergillusb. Noninfectiousi. CT diseaseii. Vasculitis
- iii. Toxic myocarditis: Toxins, medication, alcohol, cocaine, radiation therapy
Clinical features – often asymptomatica.
May present with fatigue, fever, chest pain, pericarditis, CHF, arrhythmias (inflammation affects pacemaker cells) or even death
- Diagnosisa.
ECG- abnormalities of sinus tachycardia and concave ST segment elevations
Echocardiography – ventricular dilation, reduced
EF, wall motion abnormalities
b. c. Chest radiograph – cardiac enlargement, pulmonary congestion, pleural effusion
d. Blood culturee.
Lab testsi. Increased cardiac enzymes, ESR, CRP, BNPii. Viral serology
- Treatment (depends on cause)
a. Bacterial or fungal origin – antibacterial or antifungal treatment
b. Viral – bed rest
c. Arrhythmias and heart failure with appropriate drugs
5. Prognosis
a. Most adults make a full recovery from viral myocarditisp
b. Infants have a 25% chance of survival
Rheumatic fever
Rheumatic fever is an inflammatory sequela involving the heart, joints, skin, and central nervous system (CNS) that occurs two to four weeks after an untreated infection with group A streptococcus (GAS).
The pathogenic mechanisms that cause rheumatic fever are not completely understood, but molecular mimicry between streptococcal M protein and human cardiac myosin proteins is thought to play a role.
Because of the structural similarities between the two proteins, antibodies and T cells activated to respond to streptococcal proteins also react with the human proteins, causing tissue injury and inflammation.
In addition to nonspecific symptoms (e.g., fever, malaise, and fatigue), patients present with symptoms involving the heart (pancarditis), joints (migratory polyarthritis), skin (subcutaneous nodules, erythema marginatum), and/or CNS (Sydenham chorea).
The diagnosis of acute rheumatic fever is primarily a clinical one, and is based on the Jones criteria. Diagnostic evaluation in acute rheumatic fever typically shows elevated inflammatory markers, positive antistreptococcal antibodies, and valvular damage on echocardiogram.
The first-line treatment is penicillin combined with symptomatic anti-inflammatory treatment, typically with salicylates or glucocorticoids (if salicylates are not effective).
Acute RF may be complicated by progressive, permanent damage to the heart valves (especially the mitral valve), resulting in chronic rheumatic heart disease.
Preventing the cardiac complications of rheumatic fever is the goal of both primary prophylaxis (i.e., antibiotic therapy for GAS pharyngitis) and secondary prophylaxis (antibiotic administration following an episode of acute rheumatic fever.
- Pathomechanism: after infection with streptococcus group A beta-hemolytic bacteria, the bacteria expresses a highly antigenic protein, M protein.
Our immune system mounts an immune response and creates antibodies against these proteins.
Those antibodies may cross react in cases with cells in the myocardium and heart valves.
This phenomenon, where antibodies accidently target proteins on our own cells is known as molecular mimicry, an example of type 2 hypersensitivity reaction.
- Clinical featuresa.
b. Fever, malaise, fatigue
JONES criteriai. ii. iii. iv. v.
Joints: migratory polyarthritisO (heart) – pancarditis, valvular lesions, dilated cardiomyopathy
- Pancarditis is inflammation of all layers
a. Endocardium: includes the lining of the valves, mitral and aortic commonly affected.
b. Myocardium: Aschoff cells (fibrinoid nodules) and Anitschow cells (fused macrophages)
c. Pericarditis: inflammation between visceral and parietal pericardium causes friction rub that can be heard with stethoscope.
N – subcutaneous nodules (collagen lumps)E – erythema marginatumS – Sydenham chorea (rapid involuntary movement
- Diagnosis – based on the JONES criteria and lab testsa. Complete blood cell count, ESR and CRP elevation
b. Antibody/antigen testsi.
Anti-streptolysin O
ii. Antistreptococcal DNAse B titer
c. Echocardiogram may show mitral or aortic regurgitation
4. Treatmenta. b. c. d.
Bedrest
Antibiotics (oral penicillin V)
Salicylates (Aspirin): reduce fever and relieve joint pain and swelling
Corticosteroids: improvement of joint arthritis
Pharmaceutical, interventional and surgical treatment options of acute coronary syndrome.
Infective endocarditis.
Primary and secondary prevention of myocardial infarction.
Mitral insufficiency.
myxomatous degeneration occurs.
Associated with Marfan syndrome and other CT disorders.
ii. Rheumatic fever (leaflet fibrosis occurs, does not form nice seal à blood leaks)
iii. Infective endocarditis
iv. Ischemic MR (papillary muscle rupture following acute MI)
b. Secondary (functional) MR20 – caused by changes of the left ventricle that lead to valvular incompetence, valve was normal.
i. Coronary artery disease or prior MI causing papillary muscle involvement.
ii. Dilated cardiomyopathy
iii. Left-sided heart failure leads to dilated cardiomyopathy resulting in stretching of
- mitral valve annulus allowing blood to leak into Clinical features
a. Symptoms: dyspnea, orthopnea and fatigue are the most common complaints
i. Possibly show signs of pulmonary edema or left-sided heart failure
b. Auscultation
i. Holosystolic murmur radiating to the axilla (high-pitched, blowing)
ii. Potential S3 sound
- Diagnosisa. Transthoracic echocardiography is the preferred method for diagnosis
i. LV function, LA dimensions, pulmonary pressures, and severity of regurgitation should be measured as wel
lb. c. Angiography can help assess severity American Heart Association staging of MR
- Medical therapy
Diuretics, βB, and ACEI may help improve symptoms and reduce the rate of progression
a. b. Anticoagulation therapy is indicated in patients with AF
- Indication for intervention
a. Mitral valve surgery is indicated in symptomatic patients with significant primary mitral regurgitation (grade III-IV)
b. In asymptomatic patients with significant mitral regurgitation, intervention is indicated if systolic pulmonary pressure ≥50 mmHg or LVEF ≤ 60% or LVESD ≥ 45mm or new onset of AF
- Treatmenta. Valve repair or replacement
- Special considerations in secondary regurgitationa. Surgical approach (valvuloplasty) controversial, usually used with concomitant revascularization
- b. Percutaneous edge-to-edge repair (mitral clip) improve symptoms and quality of life
Complications
a. Heart failure
b. Pulmonary edema
c. Atrial fibrillation and arterial emboli
Early and late complications of myocardial infarction.
Mitral stenosis
Differential diagnosis of chest pain.
Pacemaker treatment, CRT, ICD.
(Check table in note)
Pacemakers are implanted to help control the heartbeat.
They can be implanted temporarily to treat a slow heartbeat after a heart attack, surgery or medication overdose.
Or they can be implanted to correct a slow or irregular heartbeat or, in some people, to help treat heart failure. There are three types of pacemakers:
1) permanent implantable system for long-term treatment
2) temporary transcutaneous (with electrode pads over the chest)
3) temporary transvenous
On ECG, cardiac pacing is noted by the presence of a “spike”. Indications for pacemaker treatment are sinus node dysfunction (most common), second degree block type II, complete heart block (third degree block), symptomatic bradyarrhythmias, and tachyarrhythmias (to interrupt rapid rhythm disturbances).
Pacemakers can be classified according to the chamber being paced (stimulated), chamber sensed, response to sensing, and rate response
Pacemakers can be implanted using the endocardial or epicardial approach.
The endocardial (transvenous) approach is the most common method. A local anesthetic is given followed by an incision in the chest where the leads and pacemaker are inserted.
The lead(s) is/are inserted through the incision into a vein then guided to the heart with the aid of fluoroscopy. The epicardial approach is more common in children.
General anesthesia is given. Implantable cardioverter defibrillators (ICD): an implanted device that continuously monitors the heart and prevents sudden cardiac death by delivering electrical impulses to convert heart rhythm back into sinus rhythm.
ICDs are indicated in patients with ischemic heart disease and EF <30%, HF class II-IV patients with EF <35% and in patients with life threatening arrhythmias. Defibrillation delivers a shock that is not in synchrony with the QRS complex and works for VFib and VT without a pulse.
Cardiac resynchronization therapy (biventricular pacemaker): a three-chamber cardiac pacemaker used in symptomatic chronic HF in order to synchronize all the chambers.
It is indicated in HF class II-IV patients with EF <35%, dilated cardiomyopathy and LBBB with QRS >150 ms. It may be combined with an ICD.
Heart failure (pharmaceutical treatment, heart transplant, implantable devices: ICD, CRT, LVAD).
Toxic heart deteriorations, primary heart tumors.
Primary heart tumors
A cardiac tumor is an abnormal growth of tissue in the heart, and may be classified as either cancerous (malignant) or non-cancerous (benign).
Cardiac tumors are further classified as either primary (originating within the heart itself) or secondary (spread from a primary tumor in a different part of the body).
Primary cardiac tumors are extremely rare, occurring in approximately 1 in 3000 individuals. Seventy-five percent of primary cardiac tumors are benign.
Secondary cardiac tumors are 20-30 times more frequent than primary cardiac tumors and most commonly arise in patients with lung cancer, breast cancer, melanoma, renal cell cancer, or lymphoma.
Many patients with a cardiac tumor are asymptomatic. For patients that do have symptoms they are typically non-specific.
Symptom presentation depends primarily upon tumor location, size, growth rate, and friability (tendency to break off and travel in the blood stream).
• Clinical presentations include :
o HF, arrhythmias, chest pain, stroke, pericardial effusion, but more commonly, general symptoms such as fatigue, dyspnea, weight loss, and syncope.
• Diagnosis of cardiac tumors:Most commonly done by an echocardiogramo
o Other imaging studies such as CT, MRI, and catheterization may be done.
- Common primary tumorsa. Myxoma – most common primary tumor.
Pedunculated and have a gelatinous consistency. More likely to affect the left atrium rather than the right.
i. LA – may cause mitral stenosis and/or ii. regurgitationRA – may cause RHF
b. c. d. e. Papillary fibroelastoma – most common tumor to affect the valves.
Associated with embolization resulting in stroke. More common in left heart than right.
Rhabdomyoma – most common in infants and children. Typically, multiple and originating from the ventricular wall.
Often regress spontaneously.
Fibroma – only in infants and children.
Typically located on the ventricular wall. Associated with arrhythmias and increased risk of SCD.
Lipoma
- f. HemangiomaTreatment – in general, primary cardiac tumors require surgical resection.a. In 2-5% of patients, myxoma recurrence has been reported after resection.b. If tumors are malignant, chemotherapy should be combined with resection.
Heart failure with preserved ejection fraction.
Atherosclerosis (risk factors, pathophysiology, risk assessment, treatment), target organ
manifestations.
c. Macrophages ingest cholesterol from oxidized LDL and transform into foam cells.
a. Foam cells accumulate to form fatty streaks (early atherosclerotic lesions).
b. Oxidized LDL cannot be degraded in the macrophage.d. Platelets and endothelial cells release PDGF, FGF, TGF-alphaa.
PDGF stimulates SMC proliferation in the intima and mediates differentiation of fibroblasts into myofibroblasts.
e. Lipid-laden macrophages and SMCs produce extracellular matrix (e.g., collagen) → development of a fibrous plaque (atheroma).
f. 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 capg.
Calcification of the intima (the amount and pattern of calcification affect the risk of
- complications)h. Plaque rupture → exposure of thrombogenic material → thrombus formation with vascularocclusion or spreading of thrombogenic material
Common sites (in order of frequency)
a. Circle of Willis
b. Carotid arteries
c. Popliteal arteriesd. Coronary arteriese. Abdominal aorta
4. Risk assessment
a. SCORE24 risk charts: high and low CV risk based on gender, age, total cholesterol, systolic BP, and smoking status.
i. Calculates the 10-year CV disease risk of the patient
- Treatment
Management of risk factors
a. Medical treatment of HTN, diabetes and hyperlipidemia b. c. Interventional techniques
i. Angiography and stenting
ii. Angioplasty
iii. iv. Thrombolytic therapy Bypass surgery
- Target organ manifestations
a. Eye à retinopathy, optic neuropathy
b. Heart à coronary artery diseasec.
Brain à hypertensive encephalopathy, transient ischemic attack, stroked. Kidney à nephrosclerosis
Sudden cardiac death, cardiopulmonary resuscitation (BLS, ALS).
Acute aortic syndromes, aortic aneurysm.
(Check table in note)
- Etiology/risk factors:
Hypertension or trauma
a. In rare cases Ehlers Danlos and Marfan syndrome
b.
- Pathophysiology:
a. Transverse tear in the arterial intima leads to
i. Blood entering the intima-media space creating a false lumen
- ii. Hematoma formation that propagates longitudinally downwards
Clinical presentation and complications:
a. Sudden and severe tearing/ripping chest pain
b. Asymmetrical blood pressureSyncope, diaphoresis, confusion, agitationc.
- Diagnosis:a. Echocardiography – dissection flap, double lumen, pericardial effusion
b. CT – gold standard; dissection flap, double lumen, dilatation, hematomac. MRI – if CT is contraindicated; same findings as CT5.
d. X-ray – widened mediastinum
Treatment:
a. SurgeryImmediate for Stanford A, patients with Stanford B + complicationsi.
ii. Open surgery with replacement of the dissection with polyester graft implantation
iii. Endovascular aortic repair with stent implantation (only in Stanford B if operative risk is too high)
Aneurysms
• True aneurysms are an abnormal dilation of an artery due to a weakened vessel wall and involve all 3 layers.
Can be fusiform or saccular.
By contrast, false aneurysms are external hematomas with a persistent communication to a leaking artery, usually do to trauma (ex: gunshot, deceleration injury)
• Dissections are a separation of the arterial wall layers caused by blood entering the intimamedia 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, Iliofemoral, 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.
• Aneurysm is the second most frequent disease of the aorta after atherosclerosis.
Treatment
- Approacha.
b. Unstable patients (rupture) – emergency surgery within 90 minutes
Symptomatic patients with impeding rupture or leaking aneurysm – urgent repair within hoursc.
d. Asymptomatic patients – elective aneurysm repair or surveillance
All patients – reduction of risk factors (atherosclerosis risk factors)
- Invasive treatment
a. Endovascular aneurysm repair
i. Minimally invasive procedure that is preferred over open surgical repair for most
b. aneurysms
ii. Procedure – expandable stent graft is placed via femoral or iliac arteries Open surgical repair
i. Laparotomy is performed and the dilated segment of the aorta is replaced with a tube graft
Pharmaceutical treatment of arrhythmias.
Heart disease in pregnancy
§ For example, anticoagulation of mechanical valves during pregnancy: typically, unfractionated heparin (UFH) or LMWH in the 1st trimester, should be changed to
• vitamin K antagonists for the 2nd and 3rd trimester.
36 hours before the planned delivery, change to UFH (aPTT>2 of control).
Stop UFH 4-6 hours before operation and give back 4-6 hours after operation.
If cardiac problems do arise in pregnancy, initial diagnosis should be done with ECG and echocardiography as they are noninvasive and safe for the fetus.
If these diagnostic measures are not sufficient for a definitive diagnosis, chest radiography, CT, MRI and cardiac catheterization may be used.
Pregnancy and hypertensionHypertension in pregnancy can be divided into two major groups:
HTN with proteinuria and HTN without proteinuria.
HTN without proteinuria is further divided into pre-existing chronic hypertension and gestational hypertension; while HTN with proteinuria can either be pre-eclampsia or eclampsia.
- Gestational HTN - HTN after 20 weeks gestation in the absence of proteinuria.
It usually returns to baseline within 12 weeks of deliverya. Risk factors – chronic kidney disease, diabetes, first pregnancy, age > 40, obesity, family
b. history
Management – β-blockers and Calcium channel blockersi. ACEI/ARBs and diuretics are contraindicated
- Pre-eclampsia – widespread vascular endothelial malfunction and vasospasm, clinically defined as HTN and proteinuria (>300 mg/day) after 20 weeks gestation.
a. Risk factors – age extreme (young or old), obesity, diabetes, family history
b. Classificationi.
ii. Mild – HTN (> 140/90) + proteinuria (asymptomatic, headache, edema)
Severe – HTN (>160/110) + proteinuria + severe feature (hypertensive crisis, pulmonary edema, DIC, elevated liver enzymes, acute renal failure, hemolytic
c. anemia, and others)Management – usually deliveryi. Can give anti-hypertensive therapy: methyldopa, nifedipine, beta blockers (labetol 3. and metroprolol), hydralazine
Eclampsia – pre-eclampsia + seizures (can occur in pre-, intra-, and post-partum periods)
a. Control seizures: Prophylaxis – IV magnesium sulfate controls seizures
b. Control blood pressure: labetol, epidural analgesia to relief pain and cause vasodilation in lower extremities.
Peripartum cardiomyopathy
• Peripartum cardiomyopathy (PPCM) is a rare form of dilated cardiomyopathy (marked by LV systolic dysfunction).
o Occurs sometime between 1 month before delivery to 6 months after delivery. o It most commonly occurs right after delivery.
• The cause of PPCM is unclear but is thought to have some sort of immunological component.
• A little over half of women make a complete recovery, but recurrence in subsequent pregnancies is common (especially if cardiac function has not completely recovered.
• Signs and symptoms of PPCM are often typical for chronic HF. • Diagnosis is based on 4 criteria:
- Heart failure in the last month of gestation or within 5 months of delivery.2. Absence of other identifiable cause for HF3.
Absence of recognizable heart disease in the last month of pregnancy4. LV systolic dysfunction (EF <45%).
• Treatment is the termination of pregnancy ASAP; if it is after delivery, and is necessary, β-blockers, nitrates, and diuretics may be given.
Aortic insufficiency.
Non-pharmaceutical and pharmaceutical treatment of hypertension.
i. ii. Side effects: reduce K+ and Na+; increase glucose and cholesterol
- c. CCB (nifedipine)
i. Side effects: headache, constipation, GERDSecond-line drugsa. β-blockers (propranolol, metoprolol)
Contraindicated in patients with aortic regurgitation
i. Side effects: broncostriction and increased triglycerides
ii. b. c. d. e. Loop diuretics (furosemide)
i. Used in patients with heart failure or CKD
ii. Side effects: decrease K+ and Na+, increase glucose and cholesterolAldosterone antagonists – in patients with primary hyperaldostronism
Direct renin inhibitors – DO NOT USE WITH ACEI/ARBsAlpha-1 blockers – in patients with pheochromocytoma
- f. Direct arteriolar vasodilators – use in pregnancySteps of pharmacological treatment:
(1) Initial pharmaceutical treatment involves the combination of an ACE-inhibitor or ARB with a calcium antagonist or a diuretic (A+C/D)
(2) The second step of therapy involves the combination of an ACE-inhibitor or ARB with a calcium antagonist AND a diuretic (A+C+D)
(3) The third step of therapy involves the previous step plus 1 extra hypertensive compound (spironolactone or other diuretics, beta-blocker, alpha-blocker)– Beta blocker should be administered in case of any cardiac disorders
- Combinations
a. No two drug classes that act separately on the RAS should be used in combination.
b. Some fixed combinations are available
i. ii. iii. iv.
ACEI with CCB – Tarka (trandolapril/verapamil)
ACEI with Thiazides – Zestoretic (lisinopril/hydrochlorothiazide)
ARBs with CCB – Exforge (valsartan/amlodipine)
ARBs with Thiazides – Hyzaar (losartan/hydrochlorothiazide)
Congenital heart diseases.
Risk factors of ischemic heart disease and the treatment of risk factors.
(Check table in note)
Coartation of the aorta (CoA) – narrowing of the aorta at the aortic isthmus, which is a distal part of the aortic arch, close to the ductus arteriosus and left subclavian artery.
- Etiology – unclear
- Classification
a. Preductal (most common) – narrowing is proximal to ligamentum arteriosum
i. Right to left shunt of blood causing cyanosis due to lower pressure below
b. narrowing Postductal – narrowing is distal to ligamentum arteriosum
i. Upstream increased pressure in upper extremities and head can lead to berry
3. aneurysm
ii. Downstream decreased pressure in lower extremities à weak pulse
Diagnosis
a. Initial test – BP measurement
- b. Confirmatory – doppler echocardiography
Treatment
a. Initial managements – infusion of PGE1 (to keep ductus arteriosus open)
b. Surgical correction or balloon angioplasty for patients under
5i. Older patients may have a transcatheter intervention with stent placement
Non-invasive cardiological examinations.
Congenital heart diseases with shunt.
Congenital heart diseases with shunt
Cyanotic heart defects are congenital cardiac malformations that commonly affect the atrial or ventricular walls, heart valves, or large blood vessels.
Common causes include genetic defects, maternal infections, and maternal consumption of drugs or alcohol during pregnancy.
Pathophysiologically, cyanotic heart defects are often characterized by a right-to-left shunt, which results in deoxygenated blood entering the systemic circulation.
The resulting hypoxemia manifests clinically as cyanosis, which may occur asacute, life-threatening episodes.
Further symptoms include failure to thrive, characteristic heart murmurs, and symptoms of heart failure.
The diagnosis is confirmed by visualization via echoechocardiography. Further diagnostic findings include low oxygen saturation and characteristic X-ray findings.
Heart defects requiring treatment are repaired via catheter procedures or surgery.
Supportive medical therapy is required in cases of heart failure (e.g., diuretics, inotropic agents) or if surgery cannot be performed (e.g., prostaglandin).
If untreated, most cyanotic heart defects are fatal within the first year of life.Other conditions not talked about here:
Tricuspid valve atresia, Ebstein anomaly, hypoplastic left heart syndrome and double aortic arch.
Tetralogy of Fallot – simultaneous occurrence of 4 defects:
1) right ventricular outflow obstruction (narrowing of the valve or the infundibulum), 2) right ventricular hypertrophy, 3) VSD, 4) overriding aorta (above the VSD).
The extent of right ventricular outflow tract obstruction and central pulmonary hypoplasia determines the severity of hemodynamic dysfunction.
It is the most common cyanotic congenital heart defect (50-70%). Associated with other cardiac anomalies in 40% of patients)
1. Clinical findingsa. Cyanosis and possible oxygen saturation below 80% (depending on severity)
i. Cyanotic spells (“Tet spell”) can be reversed by squatting (increases systemic pressure and reverses the shunt)b. Clubbing of fingers and toes
- Diagnosis – Echocardiography
- Treatment – cardiac repair surgery in 1st year of lifea.
IV prostaglandins until surgery (keeps ductus arteriosus open)
Transposition of the great vessels (TGV)– anatomical reversal of the aorta and pulmonary artery. Accounts for about 20% of cyanotic congenital defects.
Often associated with VSD, left ventricular outlet obstruction, and abnormal valves/coronary arteries.
Causes are unknown but some risk factors for TGV development include diabetic mothers, alcohol consumption, age >40 and rubella infection.
- Clinical findings
a. Postnatal cyanosis, tachypnea, single loud S22. Diagnosis – echocardiography
- Treatment
a. Prostaglandins
b. Surgical correction within the first two weeks of life (without treatment 90% die within a year)
Persistent truncus arteriosus – failed separation of the aorta and pulmonary artery during development àsingle trunk that received output from both ventricles.
This is very rare condition and is sometimes associated with DiGeorge syndrome.
- Clinical featuresa. Cyanosis
b. Symptoms of HF2.
c. Harsh systolic murmur, loud S2Diagnosis – echocardiography
- Treatment – surgical repair (without treatment, 85% of patients die within the 1st year of life)
Acute left ventricular failure, pulmonary edema, cardiogenic shock (diagnosis, common causes,
treatment).
Diabetic angiopathy, „diabetic leg”.
(Check table in note)
§ Macro- angiopathy – primarily affects the large blood vessels.
Blood clots form in large o blood vessels in the brain or neck, as well as coronary arteries or large arteries of the leg. Prevent blood from reaching vital organs.
Increase the risk for heart attack or stroke.
Symptoms -depends which blood vessels is damaged
§ Micro-angiopathy of the kidney – excretion an unusually high concentration of proteins (e.g., albumin)
§ Eye- retinopathy
§ Macro angiography: weakened pulse in the early stages as well as cold feet and hands or pain when walking longer distances.
o Diagnosis
§ Diagnosis of diabetes ½
§ Doppler ultrasound can help detect blockage in the arterieso Prevention
§ Blood sugar control – daily blood sugar checks, drug therapy
§ Active lifestyleo Treatment§ Insulin injection (type 1)
§ Lifestyle changes
§ Surgical intervention
§ Removal of calcified plaque
§ Balloon catheter dilation
§ Bypass surgery
§ Stent implantation
Diabetic foot
• Diabetic foot is one of the most significant complications of diabetes, and is defined as a foot affected by ulceration that is associated with peripheral arterial disease of the lower limb in a patient with • • • diabetes.
The angiopathy results in decreased blood flow to the foot which can lead to gangrene formation and ulcers.
Due to the decreased blood flow the ulcers do not heal properly and it may take a long time.
The patient may not be aware of this because neuropathy has developed (loss of sensation).
The ulcers may become infected and abscess can form.This may cause necessary amputation of the foot or toes depending on status.
Cardiomyopathies.
Investigation of the microcirculation. Raynaud-syndrome.
• Laser Doppler measures the total local microcirculatory blood perfusion.
Light particles which hit moving blood cells undergo a change in wavelength. These are converted to electrical reading or digital imaging.
• Laser Speckle Contrast Analysis is a method that visualizes tissue blood perfusion in the microcirculation instantaneously.
Backscattered light will form a random interference pattern consisting of dark and bright areas. This pattern is called a speckle pattern.
• Transcutaneous oximetry is a local, non-invasive measurement reflecting the amount of O2 that has diffused from the capillaries, through the epidermis.
Used for determination of peripheral vascular oxygenation. Microcirculatory blood flow can exhibit vasomotion, oscillations in the vascular tone caused by changes in smooth muscle constriction and dilation.
Parameters known to influence the microcirculation are:
• Temperature
• Systemic blood pressure
• General status (stress, food, medication, smoking)
• Raynaud-syndrome
Physical activity
• It is a medical condition in which spasm of arteries cause episodes of reduced blood flow to triggers like cold or emotional stress.
Typically, the fingers, and less commonly the toes, are involved. The episodes result in the affected part turning white and then blue.
Often, numbness or pain occurs. As blood flow returns, the area turns red and burns.
• Classified as primary (idiopathic) and secondary.o Primary RP (Raynaud disease)- occurs alone§ Idiopathic, vasospasm of the digital arteries and arterioles
o Secondary RP (Raynaud syndrome)- occurs with another disease process
§ Drugs (beta, blockers)§
§ SmokingOccupational trauma§
§ Vasculitis (Buergers disease)
CT diseases (scleroderma and SLE)
• Clinical features:
o Manifestation
§ Ischemic phase (white)o o o
o § Hypoxic phase- low oxygen state after prolonged ischemia (blue)
§ Hyperemic phase (red)
Initial phase- excessive vasoconstriction, well demarcated digital pallor, cyanosis.
Subsequent phase- vasodilation, leads to intense hyperemia.
Primary RP: symmetrical, no ulceration/necrosis
Secondary RP: asymmetrical, severe pain and ulceration
• • Diagnosis: digital artery pressures are measured in the arteries of the fingers before and after the hands have been cooled.
A decrease of at least 15 mmHg is diagnostic (positive). Nail fold vasculature (capillaroscopy) can be examined under a microscope. Treatment: Calcium channel blockers (nifedipine or amlodipine)- vasodilation effect. Avoid triggers
Supraventricular arrhythmias (classification, treatment).
Obliterative arterial disease of the lower limbs (risk factors, stages, diagnosis)
o o Anticoagulant
- Warfarin reduce the risk of embolism Rate control drugs: beta-blockers (metoprolol), non-dihydropyridine calcium channel blockers (verapamil, diltiazem).
o o Cardiac glycosides (digoxin).
Catheter ablationAtrial Flutter
• Atrial flutter characterized by a sudden-onset (usually) regular abnormal heart rhythm. • It’s mostly generated by reentrant circuit that runs largely around the annulus of the tricuspid valve (right atrial tissue).
• The AV node doesn’t have time to repolarize in time, therefore not all the impulses pass through the AV node to generate a QRS complexes.
• Common conditions associated with it are hypertension, obesity, pulmonary disease (COPD).
There is absolutely regular rhythm (the distances between the QRS are equal), however more rapid than PSVT, about 250-350 bpm (atrial rate!).
• On ECG P waves are not seen, but the so called flutter waves (F-waves) are seen (saw/shark tooth pattern). 2:1 pattern à 2 F waves and 1 QRS complex (try to reduce it to 4:1 by carotid massage) o
o 4:1 pattern à 4 F waves and 1 QRS complex (more common)
• Treatment for atrial flutter:
o Should be managed the same as atrial fibrillation. Because both rhythms can lead to the formation of a blood clot in the atrium, individuals with atrial flutter usually require some form of anticoagulation or antiplatelet agent.
Both rhythms can be associated with dangerously fast heart rates and thus require medication to control the heart rate (such as beta blockers or calcium channel blockers).
Multifocal Atrial Tachycardia
• Irregular rhythm with atrial rate above 100 BPM.
• It results from the random firing of several different ectopic atrial foci.
• When the atrial rate is under 100 BPM it is called Wandering Atrial Pacemaker.
• On ECG P wave will be vary in size and shape since they are originating from multiple different fociin the atria
.• In order to diagnose MAT you need to identify at least 3 different types of P wave.
• Characteristic for COPD patient and sometimes associated with digitalis toxicity.
• In the presence of underlying pulmonary disease, the first-line agent is a non-dihydropyridine calcium channel blocker (verapamil, diltiazem).
These agents act to suppress atrial rate and decrease conduction through the atrioventricular node.
Obliterative arterial disease of the lower limbs (risk factors, stages, diagnosis)
• Most peripheral arterial diseases are atherosclerotic in origin.• PAD increases the risk of MI by 4-fold and the risk of stroke by two-to-three- fold.
• Risk factors:o Smokingo Diabetes mellituso Hyperlipidemiao Hypertension •
• When these conditions arise, there is an increase in vessel resistance that can lead to a reduction in distal artery pressure and blood flow.
Clinical manifestations of PADo Asymptomatic stage (can only be detected by screening for PAD)
o Claudication intermittens (pain after walking 200-300 meters, recovery after several minutes of rest)
o Critical limb ischemia (patient has pain at rest, cutaneous ulcers can occur)
§ Manifestation of PAD that describes patients with chronic ischemic rest pain, foot and leg ulcers, or gangrene.
§ Walking capacity very severely impaired, usually patients are incapable of walking.
• Clinical stages of PAD (Fontaine classification)o o o o o Stage 1: Asymptomatic
Stage 2a: Mild claudication
Stage 2b: Moderate to severe claudication
Stage 3: Ischemic rest pain
Stage 4: Ulceration or gangrene
• Diagnosis:
o Take thorough patient history that includes questions about risk factors and performphysical examination.
§ Inspection: changes in color of the skin of the foot, muscle atrophy, hypertrophied and slow growing nails.
§ Palpation: palpation of pulse (femoral, popliteal, dorsal pedis, posterior tibial)
o If peripheral artery disease is suspected, the initial study is the ankle–brachial index (ABI).
§ The ABI is a simple, non-invasive test, which measures the ratio of highest systolic blood pressure in the ankle to the highest systolic blood pressure in the upper arm.
§ A sphygmomanometer and a pen Doppler are used to measure the systolic BP in the dorsal pedis artery, posterior tibial artery, and the brachial artery.
§ This is based on the idea that if blood pressure readings in the ankle are lower than those in the arm, a blockage in the arteries that provide blood from the heart to the ankle is suspected.
• ABI range of 0.90 to 1.40 (NORMAL)
• ABI ≤ 0.90 (PAD)o o
• ABI < 0.5 (critical limb ischemia)If ABIs are abnormal, the next step is lower limb Doppler ultrasound (allows us to see blood flow velocity) to look at the site of obstruction and extent of atherosclerosis.
The gold standard of evaluating PAD is angiography.
• Treatment:o Lifestyle changes: stop smoking, physical activity, elimination of risk factors
o Medications:
§ Management of diabetes (metformin)
§ § Management of hypertension (ACE-inhibitors, beta-blockers)
Management of hypercholesterolemia (statins)
§ Antiplatelet drugs (aspirin and clopidogrel)§ Cilostazol: a phosphodiesterase III inhibitor, improve walking distance for people who experience claudication
• Revascularization: angioplasty, vascular bypass, amputation (in sever gangrene)
Ventricular arrhythmias (classification, treatment).
Tricuspid and pulmonary valve diseases.
Tricuspidal and pulmonary valve diseasesValvular heart diseases can take the form of stenosis, insufficiency (regurgitation), or a combination of the two.
These defects are typically acquired as the result of infections, underlying heart disease, or degenerative processes.
However, certain congenital conditions can also cause valvular heart diseases.
Acquired defects are found primarily in the left heart as a result of higher pressure and mechanical strain on the left ventricle.
The type of valvular disease determines the type of cardiac stress and subsequent symptoms.
Valvular stenosis leads to a greater pressure load and concentric hypertrophy, while insufficiencies are characterized by volume overload and eccentric hypertrophy of the preceding heart cavities.
Diagnostic procedures typically include ECGs, chest x-ray, and echocardiograms.
Management consists of interventional or surgical procedures to reconstruct or replace valves, as well as medical treatment of possible heart failure.
- Etiology – tricuspid valve defects occur in <1% of the population. Pulmonary valve defects are rare outside of congenital conditions
. Most common is secondary tricuspid regurgitation due to right ventricle dysfunction
b. following pressure and/or volume overloadPrimary tricuspid regurgitation: endocarditis [drug addicts], carcinoid syndrome, myxomatous disease, endomyocardial fibrosis, Ebstein’s anomaly
c. Tricuspid stenosis is often combined with tricuspid regurgitation, most frequently of rheumatic origin.
It is almost always associated with left-sided valve lesions, particularly mitral stenosis, that usually dominate the clinical presentationd.
Pulmonary valve problems are usually congenital. Pulmonary hypertension may cause secondary pulmonary valve insufficiency
- Clinical featuresa. Tricuspid regurgitation
i. Holosystolic murmur
- Louder with inspiration (Carvallo’s sign)ii. Right-sided HF symptoms (distended neck veins, lower extremity swelling, hepatosplenomegaly)
b. Tricuspid stenosisi. Snap and diastolic rumbleii. Right-sided HF symptoms
c. Pulmonary regurgitationi. Graham Steel murmur: high-frequency decrescendo diastolic murmurd. Pulmonary stenosis
i. Crescendo-decrescendo systolic murmurPatient evaluationa. Echocardiography is the preferred method for diagnosing tricuspidal valve problems; degree of tricuspid valve deformation, RV function, pulmonary pressures, the severity of regurgitation (grade I-IV) and transvalvular gradient should be measured
- Indication for intervention
a. Tricuspid valve surgery is indicated in symptomatic patients with significant tricuspid regurgitation or with severe tricuspid stenosis
Medical therapy
a. Diuretics are useful in the presence of HFDiagnosisa. You guessed it….echocardiogram
Treatmenta. b. c. d.
Tricuspid regurgitation – maintaining fluid balance and rarely valve repair or replacement
Tricuspid stenosis – balloon valvuloplasty
Pulmonary regurgitation – valve replacement
Pulmonary stenosis – balloon valvuloplasty
Atrial fibrillation, (pathophysiology, causes, diagnosis – manifestations, thromboembolic risk
assessment).
Buerger’s disease, Great vessel vasculitis.
o Raynaud phenomenon is often present.
Treatment: smoking cessation.
Great vessels vasculitis
The two major types of large vessel vasculitis are:
• Giant cell arteritiso affects older individuals ( > 50 age). It is also called temporal arteritis, because the temporal o artery is frequently involved.
The most frequently affected arteries are the external carotid, ophthalmic, and temporal o o o o arteries.
The underlying cause is unknown, but it might be related to helper T-cells activation.
Symptoms include: headache, jaw claudication (pain in jaw associated with chewing), scalp tenderness, visual abnormalities, fever.
Diagnosis: elevated CRP and ESR, biopsy- which involves removing a small part of the vessel under local anesthesia and examining it microscopically for giant cells infiltrating the tissuespecifically in the internal elastic lamina.
Giant cell arteritis is segmental, so take a long section of the artery.Treatment: high dose corticosteroids (prednisone) and 100 mg of ASA, methotrexate and anti-TNF therapy (ex: infliximab).
• Takayashu Arteritiso Affects younger individuals (< 50 age). Mostly Asian women are affected. o A form of large vessel granulomatous vasculitis with massive intimal fibrosis and vascular o narrowing, mainly affects the aorta and its branches, as well as the pulmonary arteries.
Symptoms include: “pulseless disease” (weaker upper extremities pulses), fever, night sweat, skin nodules, ocular disturbances.
o Diagnosis: elevated CRP and ESR, vascular lesion on magnetic resonance angiography
.o Treatment: corticosteroids (prednisone), methotrexate, azathioprine, tocilizumab (IL-6 inhibitor)
Acute and long-term treatment of atrial fibrillation.
Pericardial diseases, forms of pericarditis.
o Chest pain (severe and pleuritic)- improves on sitting and leaning forward
o Pericardial friction rib (heard on auscultation)
o Pericardial effusion (seen on chest x-ray)
• Diagnosiso Echocardiography if pericarditis with effusion is suspectedo CT/MRIo ECG§ § §
§ Diffuse ST elevation (saddle-shaped) and PR depression, with PR elevation in lead aVR.
ST segment returns to normal (typically around
1 week).T-wave inverts (does not occur in all patients).
T wave returns to normal
• Treatment
o First line: bed rest, anti-inflammatory treatment with aspirin, also omeprazole
o Second line: NSAIDs
o Third line: colchicine (treating inflammation and pain), glucocorticoids (2-4 days)
o Anticoagulants should be avoided.
Because their use could cause bleeding into the pericardial cavity and tamponade.
• Common complications: cardiac tamponade and pericardial effusion
Constrictive Pericarditis
• Medical condition characterized by a thickened, fibrotic pericardium, that forms a non-compliant shell around the heart.
This shell prevents the heart from expanding when blood enters.
• Pathophysiology:
o A fibrotic, rigid pericardium restricts the diastolic filling of the heart.
When intracardiac volume reaches the limit set by the noncompliant pericardium, ventricular filling is halted abruptly (In contrast, ventricular filling is impeded throughout diastole in cardiac tamponade).
• Causes:o Generally caused by a thickened, rigid, and fibrous pericardium secondary to acute
o pericarditis.
Other causes include uremia, radiation therapy, tuberculosis, chronic pericardial effusion, tumor invasion, connective tissue disorders, Histoplasmosis, and prior surgery involving the pericardium.
• Clinical Features:
o Symptoms of fluid overload (i.e. backward failure)§ Jugular vein distention: most prominent physical finding; indicate increase central venous pressure (CVP).
Kussmaul sign: a paradoxical rise in jugular venous pressure (JVP) on inspiration.
§ Hepatomegaly§
§ Peripheral edema and ascites
o Symptoms of reduced cardiac output (i.e. forward failure)
§ Fatigue, dyspnea on exertion
§ Pericardial knock: a high-pitched, early diastolic sound corresponding to the abrupt cessation of ventricular filling.• §
§ Diagnosis:
o ECG
§ Nonspecific changes such as low QRS voltages, generalized T-wave flattening or inversion, left atrial abnormalities.
§ AFib is more often seen in advanced disease but overall occurs in fewer than half of o o o all patients.
Echocardiogram: Increased pericardial thickness is seen in about half of all patients.
A sharp halt in ventricular diastolic filling and atrial enlargement can also be seen.
Evidence for septal bounce and reduced mitral inflow velocities with inspiration.
CT scan and MRI may also show pericardial thickening and calcifications, and can aid greatly in the diagnosis
.Cardiac catheterization§ Elevated and equal diastolic pressures in all chambers.
§ Ventricular pressure tracing shows a rapid y descent, which has been described as a dip and plateau or a square root sign.
• Treatment:
o Treat the underlying condition.
o Diuretics may be extremely helpful in treating fluid overload symptoms.
o Surgical pericardiectomy (the surgical removal of a portion or all of the pericardium).
Pericardial Effusion
• Defined as any cause of acute pericarditis (see above) that can lead to exudation of fluid into the pericardial space.
• Is often asymptomatic and suspected based on the symptoms of the underlying condition
• May be acute or chronico Acute effusions have higher risk of progressing to tamponade.
• The speed of the accumulation determines the physiologic importance of the effusion not the amount (large effusions that develop slowly may produce no hemodynamic effects;
Smaller effusions that appear rapidly can cause tamponade),
• Clinical Features:
o All physical examination signs are extremely nonspecific and often do not aid in the diagnosis but may include:
§ Muffled heart sounds
§ Soft PMI
§ Dullness at left lung base (because it may be compressed by pericardial fluid)
§ Pericardial friction rub may or may not be present
• Diagnosis:
o Echocardiogram: Imaging procedure of choice:
§ Confirms the presence or absence of a significant effusion (can show as little as 20 mL of fluid).
Should be performed in all patients with acute pericarditis to rule out an
o effusion
.Chest X-Ray:§
§ CXR shows enlargement of cardiac silhouette when >250 mL of fluid has accumulated.
Cardiac silhouette may have prototypical “water bottle” appearance.§ An enlarged heart without pulmonary vascular congestion suggests pericardial effusion
.o ECG:§
§ May show low QRS voltages and T-wave flattening but should not be used to diagnose pericardial effusion.Electrical alternans (alternating QRS amplitude) suggests a massive pericardial effusion and tamponade.
o CT scan or MR: very accurate, but often unnecessary given the accuracy of an echocardiogram
o Pericardial fluid analysis: may clarify the cause of the effusion.
§ Order protein and glucose content, cell count and differential, cytology, specific gravity, hematocrit, Gram stain, acid-fast stains, mycobacterial PCR, fungal smear, cultures, LDH content.
• Treatment:o o
o Depends on patient’s hemodynamic stability
Pericardiocentesis is not indicated unless there is evidence of cardiac tamponade.If the effusion is small and clinically insignificant, a repeat echocardiogram in 1 to 2 weeks is appropriate.
Cardiac tamponade
• The accumulation of fluid in the pericardial space in a quantity sufficient to cause serious obstruction of the inflow of blood into the ventricles results in cardiac tamponade.
This complication may be fatal if it is not recognized and treated promptly.
• Etiology – most common idiopathic pericarditis, but also may result from bleeding into the pericardial space after leakage from an aortic dissection, MI, cardiac operations, trauma (stabbing, car crash), and treatment of patients with acute pericarditis with anticoagulants.
• Clinical featureso Beck’s triad – hypotension, soft or absent heart sounds, and jugular venous distension.
o Dyspnea, orthopnea and hepatic engorgement
o Pulsus paradoxus: normally inhalation causes a tiny bit of negative pressure which pulls blood into the heart and the right ventricle expands a bit into the pericardial space due to this increase in volume.
But when we have cardiac tamponade and inhale, the right ventricle can’t move into the pericardial space so it pushes the interventricular septum leftwards causing a reduction in left diastolic volume, a lower stroke volume, and a drop in systolic pressure greater than 10 mmHg.
• Diagnosiso Echocardiogram
-TTE, TEE (see excess fluid and the heart swinging the pericardial cavity)
o ECG changes -reduction in amplitude of QRS complexes, tachycardia, and electrical alternans of the P, QRS or T waveso Doppler ultrasoundo CT
o MRI
• Treatment
o Pericardiocentesis – the pericardial effusion should be analyzed for red and white blood cells and cytologic studies, and cultures should be obtained
Abnormal impulse generation and abnormal impulse conduction (basic mechanisms, sick sinus
syndrome, SA and AV block), clinical relevance.
Anti-thrombocyte-aggregation therapy, anticoagulant and thrombolytic treatment.
in general, clot formation occurs due to 2 separate processes
- Coagulation cascade -activation of coagulation factors in order to transfer soluble
- fibrinogen to insoluble fibrin. We have 2 separate pathways – intrinsic and extrinsic.
Platelets adhesionà platelets activation à platelet aggregation.
o Therefore, in order to decrease clot formation, we have 3 methods:
© 1. Anticoagulant therapy -inhibition of intrinsic/ extrinsic coagulation cascades
- Antiplatelet therapy - inhibition of adhesion/activation/aggregation of platelets
- Fibrinolytic- enhance the lysis of fibrin clot. Anticoagulant therapo We can subdivide it into:
(1) oral anticoagulants - NOAC and vitamin K antagonists. (2) parenteral anticoagulant – heparin
- Oral anticoagulantVitamin K antagonists – warfarin §
§ Inhibit vitamin K epoxide reductase à decreased hepatic synthesis of coagulation factors 2,7,9,10, protein C and protein S.
§ Advantages
§ Well known effects and side effects
§ Low cost
§ Antidote- vitamin K and FFP
§ Disadvantages§ § § §
§ NOAC/DOACLong half lifeRegular monitoring of PT/INR required (extrinsic coagulation pathway)Broad range of interactions
Complication – skin necrosis
§ Direct oral thrombin inhibitors – Dabigatran Selective thrombin antagonists§
§ advantages§ easily management
§ regular monitoring of coagulation parameters is not
§ requiredantidote available in the case of life- threatening bleeding -idarucizumab
§ disadvantages§ costly
§ not suited for patients with valvular atrial fibrillation§ Direct oral factor Xa inhibitor -apixaban, rivaroxaban and edoxaban
Selective and direct inhibition of factor Xa § § advantages§ easily management§ regular monitoring of coagulation parameters is not required§ antidote available in the case of life- threatening bleeding -andexanet alfa
§ disadvantages
- § § parenteral anticoagulation costlynot suited for patients with valvular atrial fibrillation§ unfractionated heparin § inhibition of antithrombin
3 à inhibition of intrinsic coagulation pathway § low half life § monitoring during therapy – PTT, platelet count § antidote – protamine sulfate § complication -heparin induced thrombocytopenia § low molecular weight heparin (enoxaparin) § subcutaneous injection § in addition to UFH function, it has also anti-factor Xa activity. § Direct thrombin inhibitor ( Argatroban, bivalirudin) Intravenous administration§ © Fibrinolytic therapy o Fibrin specific agent
1. Tissue plasminogen activator (alteplase) o Non – fibrin specific agents
- Streptokinase – a protein, produced by group A streptococci, that catalyzes the conversion of plasminogen to plasmin, which is responsible for clot breakdown.
- Urokinase
o Indications
- Early STEMI
- Early ischemic shock
- Massive PE
o Contra indications
- Prior intracranial hemorrhage
- Recent surgery
- Severe hypertension
- Active bleeding© Antiplatelet therapy o Irreversible COX inhibitor (acetylsalicylic acid -aspirin)
- Indications § Acute coronary syndrome § Ischemic stroke
- § Primary and secondary prevention of cardiovascular disease
Side effects §
Aspirin exacerbated respiratory disease § GI upset § Reye syndrome o ADP receptor inhibitors (clopidogrel, prasugrel, ticagrelor)
1. Indications § Dual antiplatelet therapy (with acetylsalicyclic)
§ STEMI § Unstable angina/ NSTEMI § Before PCI § Alternative to aspirin
2. Side effect § Allergic reaction § Hemorrhaged
o Glycoprotein 2b/3a inhibitor (abciximab, eptifibatide, tirofiban)
- Indications § High risk patients with unstable angina/ NSTEMI before undergoing PCI
- Side effects § Acute thrombocytopenia § Hemorrhage.
Syncope (causes, differential diagnosis).
Obliterative arterial disease of the lower limbs (treatment forms: conservative, interventional
and surgical).
Invasive electrophysiological examination, catheter ablation.
Primary and secondary prevention in cardiology and angiology
