Diseases Of The Cardiovascular System Flashcards
1
Q
What is stable angina pectoris?
A
It is due to an atherosclerotic lesions that narrow (>70% stenosis) the major coronary arteries causing ischemia due to an imbalance between blood supply and oxygen demand.
2
Q
What are the major risk factors for stable angina pectoris?
A
- DM is the WORST RF
- Hyperlipidemia, especially high LDL
- HTN is the most COMMON RF
- Cigarette Smoking
- Age (>45 in males and >55 in females)
- Family history of premature CAD or MI in first degree relatives
- Low HDL
3
Q
What are the 3 features of typical angina heat pain?
A
- Substernal
- Worse with exertion
- Relieved with rest or nitroglycerin
4
Q
What are the different clinical presentation of CAD?
A
- Asymptomatic
- Stable angina
- Unstable angina
- MI (STEMI or NSTEMI)
- Sudden cardiac death
5
Q
How is CAD diagnosed?
A
- History
- Physical examination (Most likely to be normal)
- Resting ECG (usually normal in stable angina) + Cardiac enzymes
- Stress test (Stress ECG, Stress Echo, Stress myocardial perfusion imaging)
- Pharmacological stress test if patient can’t exercise (IV adenosine, dipyridamole, dobutamine)
- Cardiac catheterization with coronary angiography (especially if stress test is positive)
6
Q
When is a stress test considered positive?
A
If the patient develops any of the following during exercise: ST-segment depression, hypotension, chest pain, significant arrhythmias.
7
Q
How is stable angina pectoris managed?
A
- Risk factors modification
- Aspirin
- Lipid lowering agents
- Beta-blockers
- Nitrates
- CCB if b-blockers and nitrates are not fully effective
- Revascularization is indicated for stable angina refractory to medical therapy for symptom control
8
Q
What are the side effects of beta-blockers and nitrates?
A
Beta-blockers: Erectile dysfunction, inability to increase HR in response to exercise, hypotension, bronchospasm
Nitrates: headache, orthostatic hypotension, tolerance, syncope
9
Q
What is unstable angina pectoris?
A
Reduced resting coronary flow due to significant stenosis that is exaggerated by thrombosis or hemorrhage
10
Q
What are the main indications for CABG?
A
Three-vessel disease with >70% stenosis in each vessel.
Left main coronary disease with >50% stenosis, left ventricular dysfunction.
11
Q
When can we say that a patient has unstable angina?
A
- If a patient with chronic angina has increased frequency, duration, or intensity of chest pain
- Patient with new onset angina that is severe and worsening
- Patient with angina at rest
12
Q
How can we differentiate NSTEMI from unstable angina?
A
The only difference is that NSTEMI has elevation of troponin or CK-MB
13
Q
What is acute coronary syndrome (ACS)?
A
The clinical manifestations of atherosclerotic plaque rupture and coronary occlusion. It generally refers to unstable angina, NSTEMI, or STEMI.
14
Q
How is unstable angina managed initially?
A
- Hospital admission with cardiac monitoring. Establish IV access, give supplemental oxygen and pain control with nitrates and opioids.
- Dual antiplatelet therapy with aspirin and clopidogrel
- Beta-blockers
- LMWH (continued for at least 48 hours) Enoxaparin is the DOC
- Nitrates
- Glycoprotein IIb/IIIa inhibitors (helpful adjunct if patient is undergoing PCI)
- High-intensity statin
- Oxygen
- Cardiac catheterization/revascularization
- Considered if patient responds to medical therapy and a stress test is done to assess the need for catheterization/revascularization
-Considered if patient fails to respond to medical therapy
- Considered if patient responds to medical therapy and a stress test is done to assess the need for catheterization/revascularization
15
Q
What is the treatment plan after initial management?
A
- Continue aspirin life-long, clopidogrel for 1 year, beta-blockers, nitrates, and statin therapy (patients with any form of CAD should be started on statins regardless of LDL level)
- Reduce risk factors
16
Q
What is myocardial infarction?
A
Necrosis of myocardium as a results of an interruption of blood supply after a thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis
17
Q
How does MI present?
A
- Sudden onset of chest pain that is an intense substernal pressure sensation. May radiate to back, jaw, neck or arms, commonly to the left side.
- Asymptomatic
- Others include: diaphoresis, dyspnea, weakness, fatigue, nausea and vomiting, sense of impending doom, syncope.
- Sudden cardiac death.
18
Q
How can a stable angina pectoris chest pain be differentiated from MI chest pain?
A
Both have the same description of being substernal pressure sensation and radiating, but differ in duration in which stable angina lasts for 10-15 minutes and MI lasts for >30 minutes. Stable angina is related to exertion and relieved by rest or nitroglycerin and this doesn’t apply to MI.
19
Q
How is MI diagnosed?
A
ECG
Cardiac enzymes (diagnostic gold standard)
20
Q
What are the markers for ischemia/infarct on ECG?
A
- Peaked T wave: occurs very early
- ST-segment elevation: indicates transmural injury, diagnostic of acute infarct
- Q waves: Evidence of necrosis
- T waves
- ST-segment depression: indicates subendocardial injury
21
Q
Which leads represent the anterior wall and what artery supplies it?
A
V1, V2, V3, V4
Supplied by left anterior descending
22
Q
Which leads represent the lateral wall and what artery supplies it?
A
Lead I, aVL, V5, V6
Supplied by left circumflex artery
23
Q
Which leads represent the inferior wall and what artery supplies it?
A
Lead II, Lead III, aVF
Supplied by right coronary artery
24
Q
How does a posterior wall infarct appear on an ECG?
A
ST depression of V1, V2, V3, V4 (mirror image)
25
Troponin vs CK-MB
Troponin:
- increases within 3-5 hours, peaks within 24-48 hours
- returns back to normal in 5-14 days
- greater sensitivity and specificity that CK-MB
- obtain serum levels on admission and every 6 hours until 3 samples are obtained
CK-MB:
- increases within 4-8 hours, peaks within 24 hours
- returns to normal 48-72 hours
- obtain serum levels on admission and every 8 hours until 3 samples are obtained
- HELPFUL IN DETECTING RECURRENT INFARCTION
26
How is MI treated?
1. Admit to CCU, establish IV access
2. Medical therapy: Morphine, Oxygen, Nitrate, Aspirin, Beta-blockers, ACE inhibitors, Statins, LMWH (enoxaparin), Clopidogrel
3. Revascularization:
- PCI: preferred for STEMI, should be done door to balloon time less than 90 minutes
- Thrombolytic therapy: best outcome if given within the first 6 hours
- Dual antiplatelet therapy should be continued if patient undergoes PCI
4. Cardiac rehabilitation
27
What are the absolute contraindications to thrombolytic therapy?
Recent head trauma or traumatic CPR
Previous stroke within past 3 months
Recent invasive procedure or surgery
Dissecting aortic aneurysm
Active bleeding or bleeding diathesis
Severe uncontrolled HTN
Known structural cerebral lesions or neoplasm
28
What is the most common cause of death in the first few days after MI?
Ventricular arrhythmias
29
What are the complications of acute MI?
1. Congestive heart failure
2. Arrhythmias
3. Recurrent infarction
4. Mechanical complications such as free wall rupture, rupture of interventricular septum and papillary muscle rupture
5. Acute pericarditis
6. Dressler syndrome
30
What is heart failure with reduced ejection fraction?
AKA systolic dysfunction, owing to impaired contractility
31
What is heart failure with preserved ejection fraction?
AKA diastolic dysfunction, owing to impaired ventricular filling during diastole (either impaired relaxation or increased stiffness of ventricle or both.
32
How is CHF diagnosed?
1. CXR
2. Echocardiogram (initial test of choice)
3. ECG
4. B-type natriuretic peptide (released from ventricles in response to ventricular volume expansion and pressure overload)
5. Nuclear ventriculography
6. Cardiac catheterization
7. Stress testing
33
How is mild CHF (NYHA class I and II) managed?
1. Mild restriction of sodium intake
2. Loop diuretic if volume overload or pulmonary congestion is present
3. ACE inhibitor
34
How is mild to moderate CHF (NYHA Class II and III) managed?
1. Start loop diuretic and ACE inhibitor
2. Add beta-blocker if moderate disease is present and the response to standard treatment is suboptimal
35
How is moderate to severe CHF (NYHA Class III and IV) managed?
1. Add digoxin to loop diuretics and ACE inhibitors for relief of symptoms in patients with systolic dysfunction
2. Add spironolactone if EF <35%
36
What are the findings of premature atrial complexes on an ECG?
An early P wave that is different from the sinus P wave and QRS complex is normal.
37
What are the findings of premature ventricular complexes on an ECG?
Wide bizarre QRS complexes followed by a compensatory pause
38
What is the characteristic feature of AFib on ECG?
Irregularly irregular rhythm with a wavy baseline and no identifiable P waves
39
How is AFib managed in hemodynamically unstable patients?
Immediate electrical cardioversion (shock delivery that is in synchrony with QRS complex) to sinus rhythm
40
How is AFib managed in hemodynamically stable patients?
1. Rate control:
- Target HR < 110 bpm
- Beta-blockers are used
2. Anticoagulation:
- For patients with CHA2DS2VASc score > 1
- Warfarin or DOAC (Apixaban)
3. Rhythm control (cardioversion):
- Indicated if patient is unstable, patient’s first case ever, or AFib duration <48 hours
- If patient presents after >48 hours then anticoagulants for 3 weeks before cardioversion and 4 weeks after.
- OR TEE can be done to image left thrombus, if no thrombus seen the give IV heparin and perform cardioversion and continue anticoagulant for 4 weeks after cardioversion
41
What is the characteristic feature of Atrial flutter on ECG?
Saw-tooth baseline with QRS complex appearing after every second or third tooth
42
How is PSVT managed?
1. Maneuvers that stimulate vagus nerve such as valsalva maneuver, carotid sinus massage, breath holding and head immersion in cold water
2. IV adenosine
3. Prevention by CCB or Beta-blockers and ablation therapy
43
What are the ECG findings of WPW syndrome?
Narrow complex tachycardia, a short PR interval, and a delta wave
44
What are the ECG findings of ventricular tachycardia?
Wide and bizarre QRS complexes
45
How is sustained (life-threatening) VT managed?
1. If stable give IV amiodarone
2. If unstable then immediate synchronized DC cardioversion followed by IV amiodarone
3. All patient should undergo ICD placement
46
How do patients with VFib clinically present?
1. BP can’t be measured
2. No QRS complexes and no waves can be identified on ECG
47
How is VFib managed?
1. Immediate unsynchronized defibrillation and CPR are indicated
2. If persists continue CPR, may need intubation and 1 mg IV bolus epinephrine
3. If above measures fail IV amiodarone followed by shock can be done
4. If cardioversion is successful continue IV antiarrhythmic agent infusion and plan for an implantable defibrillator.
48
What is the characteristic feature of first-degree AV block?
PR interval is prolonged and a QRS complex follows each P wave
49
What is the characteristic feature of second-degree AV block?
Mobitz type I: characterized by progressive prolongation of PR interval until a P wave fails to conduct (no QRS following it)
Mobitz type II: P wave fails to conduct suddenly (no QRS following it) without a preceding PR interval prolongation
50
What is the characteristic feature of third-degree AV block?
No correspondence between P waves and QRS complexes
51
Which type of AV block requires treatment?
Second-degree Mobitz type II and third-degree AV block
52
What are the signs of hypertrophic cardiomyopathy on examination?
1. Loud S4
2. Systolic ejection murmur:
- Decreases with squatting, lying down, straight leg raise, and sustained handgrip
- Increases with valsalva maneuver and standing
3. Bisferious pulse
4. Deep T wave inversion
53
What is the definitive treatment of hypertrophic cardiomyopathy?
Heart transplant!
54
What other measures should be done when a patient is diagnosed with hypertrophic cardiomyopathy?
Screen all first degree relatives by echo.
55
What are the clinical features of acute pericarditis?
1. Pleuritic chest pain, which means that it is associated with breathing. Pain is positional in which it is aggravated by lying supine, coughing, swallowing and deep inspiration and relieved by sitting up and leaning forward.
2. Pericardial friction rub best heard during expiration with patient sitting up and stethoscope firmly placed on chest
56
What is the diagnostic criteria of acute pericarditis?
1. Classic chest pain with positional component
2. Pericardial friction rub
3. ECG changes including diffuse ST elevation and PR depression except for PR elevation and ST depression on aVR.
4. Pericardial effusion seen on CXR or echocardiogram
57
How is pericardial effusion diagnosed?
1. Clinical features are extremely non-specific
2. Echocardiogram is the procedure of choice and confirms the presence or absence of a significant effusion
3. Other tests that can be done: CXR, ECG, CT, MRI pericardial fluid analysis. These are often unnecessary due to sensitivity and specificity of echo.
58
What are the important clinical features to diagnose cardiac tamponade?
1. Beck’s triad: hypotension, muffled heart sounds, elevated JVP (prominent x descent and absent y descent)
2. Pulses paradoxus: pulse gets strong during expiration and weak during inspiration
59
What is mitral stenosis?
A diastolic murmur, in which the mitral valve is unable to open properly when it needs to be open.
60
What is the most common cause of mitral stenosis?
Rheumatic heart disease
61
What are the signs of mitral stenosis?
1. Opening snap followed by a low-pitched diastolic rumble heard best in left lateral decubitus position
2. Murmur is followed by a loud S1
62
What is the most important test to confirm MS?
Echocardiogram: showing left atrial enlargement, thick calcified mitral valve, narrow (fish mouth shaped orifice)
63
What is the most common type of valvular disease?
Aortic stenosis
64
What are the signs of aortic stenosis?
1. Harsh crescendo-decrescendo systolic murmur that radiates to carotid arteries and lower left sternal border
2. Soft S2
65
What is the treatment of choice for aortic stenosis?
- If asymptomatic then no treatment
- If symptomatic aortic valve replacement is the treatment of choice
66
What are the clinical feature of aortic regurgitation that are seen on physical examination?
1. Widened pulse pressure
2. Diastolic decrescendo murmur heard best at left sternal border, intensity increases with sustained handgrip. Increases by leaning forward and expiration
67
What are the clinical features of mitral regurgitation?
Holosystolic murmur at the apex, which radiates to the back or clavicular area
68
What is the management plan for mitral regurgitation?
1. Medical: to reduce after load by vasodilators or IABP because this allows ventricles to prefer pumping into the low pressure aorta than back to atrium.
2. Mitral valve replacement or repair
69
What is rheumatic heart disease?
Occurs as a complication of streptococcal pharyngitis (Group A streptococcus).
70
How is acute rheumatic fever diagnosed?
It requires 2 major criteria or one major and 2 minor
1. Major criteria includes:
Joint involvement (migratory polyarthritis)
O= Cardiac involvement
Nodules (subcutaneous)
Erythema marginatum
Sydenham chorea
2. Minor criteria includes:
CRP (elevated)
A = Polyarthralgia
Fever
ESR (elevated)
PR interval (prolonged)
Anamnesis of rheumatism (prior history)
Leukocytosis (evidence of preceding streptococcal infection)
71
What is infective endocarditis?
Proliferation of microorganisms on the endothelial surface of the heart.
72
What is the most common cause of acute endocarditis?
Staphylococcus aureus (highly virulent) that occurs on a normal heart valve
73
What is the most common cause of native valve endocarditis?
Streptococcus viridans
74
What is the most common cause of early-onset prosthetic valve endocarditis?
Staphylococcus epidermidis
75
How is infective endocarditis diagnosed?
1. Transthoracic echocardiography and transesophageal echocardiography
2. ECG
3. CXR
4. Urinalysis
MUST fulfill Duke clinical criteria: 2 major, 1 major and 3 minor, or 5 minor criteria
76
How is infective endocarditis managed?
1. 3 sets of blood cultures should be drawn prior to initiating antibiotic therapy
2. Parenteral antibiotics based on culture for 4-6 weeks: (nafcillin-penicillin or vancomycin) + gentamicin
3. If patient has any intracardiac device it must be removed
77
What procedures qualify for endocarditis prophylaxis and what is given?
1. Dental procedures involves bleeding or manipulation of tissue
2. Procedures involving biopsy or incision of respiratory mucosa
3. Procedures involving infected skin or musculoskeletal tissue
Amoxicillin is commonly used, but choice depends on site of procedure
78
What is aortic dissection?
A tear in the inner layer of the aorta that leads to a progressively growing hematoma in the intima-media space.
79
What is the most common predisposing factor for aortic dissection?
Long-standing systemic HTN
80
How does aortic dissection present?
Severe, tearing/ripping/stabbing pain, typically abrupt in onset, either anterior or back of the chest.
81
How is aortic dissection diagnosed?
1. CXR showing widened mediastinum
2. CT angiogram and MRI (both are highly accurate)
3. Transesophageal echocardiography
82
What is the management plan for aortic dissection?
1. Immediately initiate medical therapy with beta-blockers to reduce HR and BP (systolic BP goal 100-120 ASAP)
2. Type A (ascending aorta) is treated surgically
3. Type B (descending aorta) is treated medically
83
What is abdominal aortic aneurysm?
Abnormal localized dilation of the aorta
84
What are the clinical feature of ruptured AAA?
Triad of abdominal pain, hypotension, and a palpable pulsatile abdominal mass and an emergent laparotomy is indicated.
85
What is the test of choice to diagnose AAA?
Ultrasound
86
How is AAA managed?
1. Unruptured: if >5 cm in diameter or symptomatic, surgical resection with synthetic graft placement is recommended. If <5 cm still is at risk of rupture , so it is recommended to follow up growth to assess risk.
2. Ruptured: requires emergency surgical repair
87
What are the signs and symptoms that are common to all forms of shock?
1. Hypotension
2. Oligouria
3. Tachycardia
4. Altered mental status
88
What is cardiogenic shock?
Occurs when the heart is unable to generate a cardiac output sufficient to maintain tissue perfusion. It can be defined as a systolic BP <90 with urine output <20 mL/hr and adequate left ventricular filling pressure.
89
What are the hemodynamic changes in cardiogenic shock?
1. Decreased cardiac output
2. Increased SVR
3. Increased PCWP
4. Elevated JVP
90
What are the hemodynamic changes in hypovolemic shock?
1. Decreased cardiac output
2. Increased SVR
3. Decreased PCWP
91
What is the most useful indicator of the effectiveness of treatment in shock?
Urine output
92
What is septic shock?
Type of distributive shock characterized by hypotension induced by sepsis that persists despite adequate fluid resuscitation. This results in hypoperfusion and can ultimately lead to multiple organ system failure and death.
93
What are the hemodynamic changes in septic shock?
1. Increased cardiac output
2. Decreased SVR secondary to peripheral vasodilation, extremities are often warm
3. Decreased PCWP
94
What is neurogenic shock?
A type of distributive shock, results from failure of the sympathetic nervous system to maintain adequate vascular tone.
95
What are the hemodynamic changes in neurogenic shock?
1. Decreased cardiac output
2. Decreased SVR secondary to peripheral vasodilation, extremities are often warm
3. Decreased PCWP
96
What are the hemodynamic changes in obstructive shock?
1. Decreased cardiac output
2. Increased SVR
3. Variable PCWP
4. Elevated JVP
