Cardiology Flashcards
(82 cards)
1
Q
Risk factors for stabile angina pectoris (SAP)
A
Diabetes = worst risk factor Hypertension = most common risk factor Hyperlipidemia - elevated LDL Smoking Age (men > 45, women >55) Low HDL-levels Family history of CAD, especially 1st degree (Minor: obesity, lifestyle, stress, alcohol)
2
Q
Prognostic indicators of CAD
A
1) Left ventricular function/Ejection fraction < 50% -> assoc. with increased mortality
2) Left main coronary artery - poor prognosis b.c it covers approx. 2/3 of the heart
3) Two- or three-vessel CAD - worse prognosis
3
Q
What is the LDL goal in a patient with CAD?
A
LDL less than 100 mg/dL
4
Q
Metabolic syndrome =
A
A cluster of conditions that occur together (hypercholesterolemia, hypertriglyceridemia, impaired glucose tolerance, diabetes, hyperuricemia, HTN), increasing your risk for CAD, stroke and Diabetes. Key underlying factor is insulin resistance (due to obesity).
5
Q
Syndrome X =
A
Exertional angina with normal coronary arteriogram. Patients present with chest pain after exertion, but have no coronary stenosis at cardiac catherization. Excercise testing and nuclear imaging show evidence of myocardial ischemia.
6
Q
Standard of care for stable angina
A
Aspirin and a B-blocker (only ones that lower mortality), and nitrates for chest pain.
7
Q
Function of B-blockers
A
Block sympathetic stimulation of heart. First line choices include Atenolol and metoprolol. Reduces HR, BP and contractility, thereby decr. cardiac work(i.e oxygen consumption)
8
Q
Management of mild stable angina (normal EF, mild angina, single-vessel disease)
A
1) Aspirin + Risk factor modification (Indicated in all)
2) B-blocker
3) Nitrates (for Sx and prophylaxis)
4) Consider calcium channel blockers if Sx continue despite nitrates and B-blockers.
9
Q
Management of moderate stable angina (normal EF, moderate angina, two-vessel disease)
A
1) Aspirin + Risk factor modification (Indicated in all)
2) B-blocker
3) Nitrates (for Sx and prophylaxis)
4) Consider calcium channel blockers if Sx continue despite nitrates and B-blockers.
- If the above regimen does not control Sx, consider coronary angiography to assess suitability for revascularization (either PCI or CABG)
10
Q
Management of severe stable angina (decreased EF, severe angina, three-vessel/left main or left anterior descending disease)
A
Coronary angiography and consider for CABG
11
Q
“Acute Coronary Syndrome” =
A
The clinical manifestation of atherosclerotic plaque rupture and coronary occlusion. Term generally refers to USA, NSTEMI or STEMI.
12
Q
What is the main difference between SA and USA?
A
With USA, oxygen demand is unchanged. Supply is decreased secondary to reduced resting coronary flow. This is in contrast to stable angina, which is due to increased demand.
13
Q
What is the distinction between USA and NSTEMI?
A
The distinction between USA and NSTEMi is based entirely on cardiac enzymes. The latter has elevation of troponin or creatine kinase-MD (CK-MB). Both USA and NSTEMI lack ST-segment elevations and pathologic Q-waves.
14
Q
Treatment of USA
A
Aggressive medical Mx is indicated - treat as in MI except for fibrinolysis.
A) Aspirin
B) Plavix/Clopidogrel
C) B-blockers - first line therapy if no contraindications
D) LMWH (Enoxaparin)- superior to unfractionated heparin - should be given for at least 2 days
E) Nitrates
F) O2
G) Glycoprotein IIb/IIIa inhibitors
H) Morphine (controversial bc can mask Sx)
I) Replacement of deficient electrolytes, espec. K+ and Mg2+
PS: Pts. w/USA should be treated w/Aspirin and Plavix for 9-12months, but may be altered according to bleeding-risk.
If no improvement of Sx or on ECG after 48h –> Catheterization/revascularization
After acute Tx: Aspirin/or other antiplatelet-therapy, B-blockers and nitrates + reduce RF
15
Q
Variant (Prinzmetal) Angina =
A
Transient coronary vasospasm
Uually accompanied by a fixed atheroslerotic lesion, but can occur in normal coronary arteries.
Episodes occur at rest, often at night, and are assoc. w/ventricular dysrrhytmias.
Hallmark: Transient ST-segment elevation (not depression) on ECG during rest.
Def. test: Coronary angiography with given IV ergonovine or acetylcholine to provoke vasoconstriction.
Give vasodilators: Ca-channel blockers and nitrates.
16
Q
Mechanism of MI
A
Necrosis of myocardium. Most cases are due to acute coronary thrombosis: Atheromatous plaque ruptures into the vessel lumen, and thrombus forms on top of this lesion, which causes occlusion of the vessel.
17
Q
Markers for ischemia/infarction on ECG
A
- Peaked T-waves: Occur early and may be missed
- ST-segment Elevation: Indicates transmural injury and can be diagnostic of an acute infarct.
- Q-waves: Evidence for necrosis (specific) - Q-waves are usually seen late, typically not acutely
- T-wave inversion: sensitive, but not specific
- ST-segment depression: Subendocardial injury
18
Q
ECG findings based on location of infarct
A
Anterior:
ST-segment elevation in V1-V4
Q-waves in leads V1-V4 (late change)
Posterior:
Large R-wave in V1 and V2
St segment depression in V1 and V2
Upright and prominent T-waves in V1 and V2
Lateral:
Q-waves in leads I and aVL (late change)
Inferior:
Q-waves in leads II, III and aVF (late change)
19
Q
STEMI vs NSTEMI (location)
A
STEMI: Transmural (involves entire thickness of wall, tends to be larger.
NSTEMI: Subendocardial (involves inner one-third to one-half of the wall), tends to be smaller, and presenttion is similar to USA, cardiac enzymes differentiate the two.
20
Q
The Cardiac enzymes
A
- Troponins (Best)
Increases within 3-5h and returns to normal in 5-14d; reaches a peak in 24-48h. Obtain on admission and every 8h for 24h. - CK-MB
Increases within 4-8h and returns to normal in 48-72h, reaches a peak within 24h. Measure on admission and every 8h for 24h. More helpful in detecting recurrent infarction given quicker return to baseline than troponin.
21
Q
Initial tx of MI
A
A) Aspirin B) B-blockers C) ACE-inhibitors D) Statins E) O2 F) Nitrates G) Morphine H) Heparin
Then Revascularization:
Benefits highest if performed early(within 90min of arrival)
Options include PCI, thrombolysis or CABG
PCI is the gold standard, but fibrinolysis alone may be the best option for delayed presentation. CABG if complicated MI(cardiogenic shock, life threatening v.tac, or after failure of PCI).
22
Q
Dressler syndrome/Postmyocardial infarction syndrome =
A
Immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis and peuritis. Occuring weeks to months after an MI. Aspirin as treatment.
23
Q
Congestive Heart failure - what is the difference between systolic and diastolic dysfunction?
A
Systolic dysfunction: Owing to impaired contractility (i.e the abnormality is decr. EF).
Diastolic dysfunction: Owing to impaired ventricular filling during diastole.
24
Q
Causes of systolic dysfunction CHF
A
Ischemic heart disease/after MI
HTN resulting in cardiomyopathy
Valvular heart disease
Myocarditis (postviral)
25
Causes of diastolic dysfunction CHF
HTN leadning to myocardial hypertrophy - mostcommon
Valvular diseases such as aortic stenosis, mitral stenosis
Restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemochromatosis)
26
Sx of Left sided heart failure
Dyspnea - secondary to pulm congestion
Orthopnea - difficulty breathing in the recumbent position
Paroxysmal nocturnal dyspnea
Nocturnal cough
Confusion and memory impairment - result of inadequate brain perfusion
Diaphoresis and cool extremities at rest
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Signs:
Pathologic S3
S4 gallop
Cracles/rales
Dullness to percussion
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27
Sx of Right sided heart failure
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Peripheral pitting edema
Nocturia - due to incr. venous return with elevation of legs
Jugular venous distention
Hepatomegaly/hepatojugular reflux
Ascites
Right ventricular heave
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28
Diagnosis of CHF
Most important:
1. Chest X ray
- Cardiomegaly
- Kerley B-lines (indicate pulm. congestion)
- Pleural effusion
2. Echocardiogram
- can differentiate between syst. or diast. failure
- Estimates EF (syst.failure: EF<40%).
- shows chamber dilation or hypertrophy
29
Treatment of CHF
Systolic dysfunction:
1. Lifestyle modification
2. Diuretics (Lasix/Loop diuretics most common)
3. Spironolactone (only for advanced)
4. ACE inhibitors (The combo of a diuretic and an ACE inhibitor should be the intitial tx in symptomatic pts.)
5. B-blockers (Proven to decr. mortality in pts. with post-MI heart failure)
6. Digitalis - (For patients with EF < 40%, who continue to have symptoms despite standard therapy)
Diastolic dysfunction:
1. B-blockers
2. Diuretics
3. Spironolactone and Digoxin should NOT be used.
- NO medications have proven mortality benefit
30
Arrhytmias : Premature Complexes :
| Premature Atrial Complexes
Early beat arising from atria, firing on its own. Found in 50% of people. Usually normal, may be a precursor of ischemia in diseased heart.
Causes: adrenergic excess, coffee, drugs, alcohol, electrolyte abn. etc.
ECG: Early P waves that differ in morphology from normal P wave. QRS normal.
Tx: Nothing. If very symptomatic - B-blockers.
31
Arrhytmias: Premature Complexes:
| Premature Ventricular complexes
Early beat that fires on its own from a focus in the ventricle. Can occur in patients with or without structural heart disease. Can occur in 50% of people, presence of PVCs in pts with normal hearts is assoc. with incr. mortality. Workup is necessary. (Can cause arrhytmias)
Causes: hypoxia, electrolyte abn, stimulants, caffeine etc.
ECG: Wide, bizarre QRS complexes followed by a compensatory pause, P-wave often buried in the QRS-complex.
Tx: If symptomatic, B-blockers. If frequent PVCs: workup.
32
Tachyarrhytmias:
| Atrial fibrillation
Multiple foci in atria fire continuously in a chaotic pattern -> irregular, rapid ventricular rate. Rate between 75 and 175. Markedly incr. risk of thromboembolism + hemodynamically compromise. Irregularly irregular pulse.
ECG: Irregular RR intervals, excessively rapid series of tiny, erratic spikes on ECG with a wavy baseline and no P-waves.
Treatment:
Unstable: Electrical cardioversion
Stable: 1) Rate control(B-blockers - target rate 60-100)
2) Anticoagulate pts. for 3 weeks OR TEE to check for thrombus in atrium then --> Cardioversion to sinus rhytm (after rate control achieved). INR of 2-3 is best.
33
Tachyarrhytmias:
| Atrial flutter
One irritable automaticity focus in the atria fires at around 300bpm.
ECG: Saw-tooth baseline (best seen in II, II, avF
Tx: Similar as Afib
34
Paroxysmal Supraventricular Tachycardia
= AV-nodal reentrant tachycardia OR Orthodromic AV reentrant tachycardia
Av-nodal is the most common cause of supraventricular tachyarrhytmia. Initiated or terminated by PACs
ECG: Narrow QRS-complexes with no discernible P waves (P-waves buried within QRS).
35
Treatment of Paroxysmal Supraventricular Tachycardia
1. Maneuvers that stimulate the vagus delay and block the reentry mechanism: The valsalva maneuver, carotid sinus massage, breath holding etc.
2. IV adenosine - agent of choice due to short duration of action and effectiveness in terminating SVT.
3. Prevention: Verapamil or B-blockers
36
Wolff-Parkinson-White Syndrome
An inborn acessory conduction pathway from atria to ventricles through the "Bundle of Kent". Causes premature ventricular excitation because it lacks the delay seen in the AV-node. May lead to a paroxysmal tachycardia, which can be produced by 1) Orthodromic reciprocating tachycardia, 2) Supraventricular tachycardias (Afib or flutter).
ECG: narrow complex tachycardia, short RR-interval, and a delta wave.
Tx: Radiofrequency catheter ablation of reentrant loop+ Procainamide or quinidine
37
Ventricular tachycardia
Rapid and repetitive firing of three or more PVCs in a row. Range: 100-250bpm. AV-dissociation is present, sinus P waves continue with their cycle, unaffected by the tachycardia.
```
Sustained vs nonsustained VT:
1) Sustained:
Lasts longer than 30 seconds and is almost always symptomatic. Often hemodynamically comprise (hypotension), MI etc. Life threatening, can progress to Vfib.
2) Nonsustained:
Brief, self-limited runs of VT
Usually asymptomatic
Should be followed up
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38
Ventricular tachycardia - clinical and ECG
1. Palpitations, dyspnea, lightheadedness, angina, syncope
2. May present with sudden cardiac death
3. Signs of cardiogenic shock may be present
4. May be asymptomatic if rate is slow
5. Physical findings include cannon A waves in the neck
ECG:
Wide and bizarre QRS complexes
Unlike PSVT, VT does not respond to vagal maneuvers or adenosine
39
Ventricular tachycardia - treatment
Sustained VT:
1) Hemodynamically stable patients with mild symptoms and systolic BP > 90 - Pharmacologic treatment - IV amiodarone, IV Procainamide or IV sotalol
2) Hemodynamically unstable patients or patients with severe symptoms
- Immediate synchronous DC cardioversion
- Follow with IV amiodarone to maintain sinus rhytm
40
Ventricular fibrillation
Multiple foci in the ventricles fire rapidly, leading to a chaotic quivering of the ventricles and no cardiac output.
- Most episodes of VFib begin with VT (exept in the setting of acute ischemia). Fatal if untreated.
Ischemic heart disease is the most common cause
Clinical: Cannot measure BP, absent heart sound and pulse. Unconscious patient. If untreated -> death
ECG: No atrial P waves, No QRS-complexes, very irregular rhytm
41
Ventricular fibrillation - Treatment
Medical emergency - Immediate defibrillation and CPR are indicated. Give up to 3 sequential shocks to establish another rhytm.
Intubation may be indicated
Epinephrine (1 mg IV bolus initially, then every 3-5min)
If still nothing, IV Amiodarone 300mg, then 150mg
42
Bradyarrhytmias: Sinus arrhytmia (What?, Causes, Tx)
Sinus rate < 60 bpm, significant if <45bpm
Causes: Ischemia, vagal tone, antiarrhytmic drugs, trained athletes
Tx: Atropine can elevate the sinus rate by blocking vagal stimulation to the SA node.
43
Bradyarrhytmias: Sick sinus syndrome (What? Sx, Tx)
Sinus node dysfunction characterized by a persistent spontaneous sinus bradycardia. Pts. usually elderly.
Sx: dizziness, confusion, syncope, fatigue, CHF
Pacemaker-implantation may be required.
44
AV Block: First degree AV Block - ECG?
PR-interval is prolonged (>0,2 second)
A QRS complex follows each P wave
Delay is usually in the AV node
Does not require treatment
45
AV Block: Second-degree AV block (Include Mobitz type I and II)
1. Mobitz type I (Wenckebach)
- Characterized by progressive prolongation of PR interval until a P wave fails to conduct
- Site of block is usually within the AV node
- Benign condition, does not require tx
2. Mobitz type II
- P wave fails to conduct suddenly, without a preceding PR interval prolongation; therefore, the QRS drops suddenly, without a preceding PR interval prolongation, therefore the QRS drops suddenly.
Site of blocks is within the His-Purkinje system.
Pacemaker implantation is necessary
46
AV Block: Third-degree (complete) AV block
Absence of conduction of atrial impulses to the ventricles: no correspondence between P waves and QRS complexes.
A ventricular pacemaker (escape rhytm) maintains a ventricular rate of 25-40 bpm. Characterized by AV dissociation. Pacemaker is necessary.
47
Diseases of the heart muscles: Dilated cardiomyopathy (General, Causes)
General: Most common type of cardiomyopathy. An insult (ischemia, infection, alcohol etc) causes dysfunction of left ventricular contractility. Poor prognosis - many die within 5 years of the onset.
Causes: 50% idiopathic. Other: CAD, Toxic, Metabolic, Infection etc.
48
Diseases of the heart muscles: Dilated cardiomyopathy (Clinical, diagnosis, Tx)
Clinical:
Sx and sign of left- and right sided CHF develop
S3 and S4 and murmurs of mitral or tricuspid insufficiency may be present
Cardiomegaly commonly seen
Dx:
ECG, CXR andechocardiogram results consistent with CHF.
Tx: Similar to tx of CHF: Digoxin, diuretics, vasodilators
49
Diseases of the heart muscles: Hypertrophic Cardiomyopathy (General, Clinical)
Most cases are inherited (autosomal dominant).
The main problem is diastolic dysfunction due to a stiff, hypertrophied ventricle with elevated diastolic filling pressures.
Clinical: Sx:
Dyspnea, chest pain, Syncope, Palpitations, Arrhytmias, Cardiac failure, Sudden death
Signs: Sustained PMI, Loud S4, Systolic ejection murmur
50
Diseases of the heart muscles: Hypertrophic Cardiomyopathy (Diagnosis and Treatment)
Dx: Echocardiography
Tx: Asymptomatic patients generally do not need treatment, but should avoid strenous exercise.
Symptomatic patients: B-blockers, Ca-channel blockers (Verapamil), Diuretics.
51
Diseases of the heart muscles: Restrictive Cardiomyopathy (General, Causes, Clinical, Dx, Tx)
General: Infiltration of the myocardium results in impaired diastolic ventricular filling due to decr. ventricular compliance. Systolic dysfunction is variable. Less common than dilated and hypertrophic cardiomyopathies.
Causes: Amyloidosis, Sarcoidosis, Hemochromatosis, Scleroderma, Carcinoid syndrome etc.
Clinical: Elevated filling pressure causes dyspnea and exercise intolerance.
Dx: Echo: Thickened myocardium + systolic ventricular dysfunction. Increased RA and LA, normal LV and RV size.
Tx: Treat underlying disorder:
Hemochromatosis: Phlebotomy or deferoxamine
Sarcoidosis: glucocorticoids
Etc.
52
Myocarditis
Inflammation of myocardium.
Causes: Viruses (e.g Coxsackie, Parvovirus, HHV-6), Bacteria (Group A strep, Lyme, mycoplasma), SLE,medications.
May be asymptomatic, may present with fatigue, fever, chest pain, pericarditis, CHF, arrhytmia, death.
The classic patient is a young male.
Look for elevations in cardiac enzyme levels and ESR
Tx: supportive.
53
Pericardial diseases: Acute Pericarditis (General)
```
Inflammation of the pericardial sac.
Causes:
Idiopathic (probably postviral).
Infectious (Viral(Coxsackievirus, echovirus, adenovirus), Bacterial(TB), fungal, toxo
Acute MI
Uremia
Collagen vascular diseases
Etc.
```
- The majority of patients recover within 1-3 weeks. A minority of pts have a prolonged course or recurrent symptoms.
Cx: Pericardial effusion, cardiac tamponade
54
Pericardial diseases: Acute Pericarditis (Clinical)
1. Chest pain (most common) often assoc. w/breathing(pleuritic pain), often localized retrosternal and radiates to trapezius.
2. Pain is positional: it is aggravated by lying supine, coughing, swallowing and deep inspiration. Pain is relieved by sitting up and leaning forward.
Fever and leukocytosis may be present
Patient may give sx of preceding viral illness
Pericardial friction rub - not always present, but is very specific for pericarditis.
55
Pericardial diseases: Acute Pericarditis (Dx and Tx)
Dx: ECG: Diffuse ST-elevation and PR-depression. Inverted T-wave
Tx: Most cases areslef-limited and resolve within 2-6w. NSAIDS are mainstain of therapy. Colchicine also often used.
56
Pericardial diseases: Constrictive Pericarditis (General, Clinical, signs)
Fibrous scarring of the pericardium leads to rigidity and thickening of the pericardium, with obliteration of pericardial activity.
In most pts. the cause is never identified, but can include uremia, radiation therapy, TB etc.
Clinical: Patient appear very ill,
1) With sx characteristic of fluid overload
2) With sx related to the diminished cardiac output, such as dyspnea, fatigue, decr. exercise intolerance
```
Signs:
JVD - most prominent physical finding.
Kussmaul sign - JVD
Pericardial knock
Ascites
Dependent edema
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57
Pericardial diseases: Pericardial Effusion - General and Clinical
Defined as any cause of acute pericarditis that can lead to exudation of fluid into the pericardial space. Can occur in assoc. w/ascites, pleural effusion in salt and water retention, i.e CHF, cirrhosis etc. Often asymptomatic.
Clinical: Extremely nonspecific
a) muffled heart sounds
b) soft PMI
c) Dullness at left lung base
d) Pericardial friction rub may be present
58
Pericardial diseases: Pericardial Effusion - Dx and Tx
Dx: Echocardiogram - confirms presence or absence of effusion. CXR - shos enlargement of cardiac silhouette, the typical "water bottle" appearance.
Tx: Depends on hemodynamically stability
Pericardiocentesis not indicated unless there is evidence of cardiac tamponade.
59
Cardiac Tamponade - General and Clinical
Accumulation of pericardial fluid - it is the rate of fluid accumulation that is important, not the amount.
--> Pericardial effusion that mechanically impairs diastolic filling of the heart.
Ventricular filling is impaired during diastole.
Causes: Penetrating trauma to thorax, sch as gunshot and stab wounds. Iatrogenic: Central line placement, pacemaker insertion f.eks, Pericarditis: Idiopathic, neoplastic, Post MI.
Clinical: Elevated jugular venous pressure is the most common finding(distended neck veins). Narrowed pulse pressure. Pulsus paradoxus, Distant(muffled) heart sounds, tachypnea, tachycardia, hypotension.
60
Cardiac tamponade - Dx and Tx
Echocardiogram - usually diagnostic
CXRAY - Enlarged cardiac silhouette when > 250ml acummulated
```
Tx:
1) Nonhemorrhagic tamponade:
If pt. is hemodynamically stable: Monitor closely. If pt. has known renal failure, rather do dialysis than pericardiocentesis.
If pt. is hemodynamically unstable:
Periocardiocentesis is indicated
```
2) Hemorrhagic tamponade:
If bleeding is unlikely to stop on its own, emergent surgery. Pericardiocentesis is only a temporizing measre and is not definite tx.
61
Valvular heart disease: Mitral stenosis (General)
Almost all are due to Rheumatic heart disease (Immune mediated damage to mitral valve due to cross-reactivity -> scarring and narrowing of mitral valve orifice.
Narrowing results in elevated left atrial and pulm. venous pressure -> pulm. congestion. Long standing can result in pulm HTN and Right ventricular failure. Afib can occur due to increased size + pressure.
62
Valvular heart disease: Mitral stenosis (Clinical + Signs + Dx + Tx)
```
Exertional dyspnea, orthopnea, PND
Palpitations, chest pain
Hemopthysis (elevated pressure ruptures small bronchial veins)
Thromboembolism - assoc. w/Afib
If RVF occurs -> ascites + edema
```
Signs: S2 is followed by an opening snap. Murmur is followed by loud S1
Dx:
CXR : enlarged atrial enlargement
Echo: most important test in diagnosis - LA enlargement, thick, calcified mitral valve. Narrow "fish mouth" orifice of MV.
Tx: Medical or surgical if bad
Medical: Diuretics + B-blockers
Surgical: Baloon valvuloplasty
63
Valvular heart disease: Aortic Stenosis (General, Causes, signs, clinical, Dx, Tx)
Calcification of a congenitally abnormal bicuspid aortic valve OR calcification of tricuspid valve in elderly OR rheumatic fever.
Causes obstruction to LV outflow -> left ventricular hypertrophy. With long-standing AS, the LV dilates -> progressive LV dysfunction + dilation pulls the mitral valve annulus apart, causing MR.
Signs: Harsh crescendo-decrescendo systolic murmur. Soft S2. S4. Parvus et tardus (diminished and delayed carotid upstrokes)
Clinical: Patients often asymptomatic for years. Angina, syncope, heart failure -> poor prognosis.
Dx: CXR: Calcific aortic valve, enlarged LV/LA
Ecg: LVH, LA abnormality
Echo: diagnostic in most cases -> LVH, thickened immobile AV, dilated aortic root
Tx: Surgical therapy: aortic valve replacement is tx of choice. Indicated in all symptomatic pts.
64
Valvular heart disease: Aortic regurgitation (General, causes, Clinical, Dx, Tx)
Also called aortic insuff. Inadequate closure of the aortic valve leaflets. Regurgitant blood floow incr. LVEDV -> LV dilation and hypertrophy -> incr left sided and pulm pressure.
Causes:
1) Acute: Infective endocarditis, trauma, aortic dissection, iatrogenic
2) Chronic: Primary valvular: Rheumatic fever, bicuspid aortic valve, Marfan, Ehler Danlos etc. Aortic root disease
Clinical: May be symptomatic for many years (dyspnea, palpitations, angina, cyanosis)
Signs: Widened pulse pressure, markedly increased systolic BP, with decreased diastolic BP. Diastolic decrescendo murmur. Corrigan pulse (water-hammer pulse) Austin Flint murmur.
Dx: CXR: LVH, dilated aorta
Echo: assess LV size and function, look for aortic root and reversal of blood flow in aorta.
Tx: If asymptomatic: conservative w diuretics, vasodilators, digoxin, ACE-inhibitors.
Definite tx is aortic valve replacement. If acute AR (e.g post-MI): Medical emergency! perform emergent aortic valve replacement.
65
Valvular heart disease: Mitral regurgitation (General, causes, clinical)
Acute: Abrupt elevation of left atrial pressure in the setting of normal LA size and compliance, causing backflow into pulm.circulation with resultant pulm.edema. Cardiac output decr. b/c of decr. forward flow, so hypotension and shock can occur.
Chronic: The same, but more "chronically"
```
Causes:
Acute: Endocarditis (Staph.Aureus)
Papillary muscle rupture or dysfunction
Chordae tendineae rupture
Chronic: Mitral valve prolapse
Rheumatic fever
Marfan syndrome
Cardiomyopathy
```
Clinical: Dyspnea, PND, ortophnea, palpitations, pulm. edema.
66
Valvular heart disease: Mitral regurgitation (Signs, Dx, Tx)
Holosystolic murmur at the apex
Afib common finding
DiminishedS1, widening of S2, S3 gallop
Dx:
CXR: Cardiomegaly, dilated LV, pulm edema
Echo: MR, dilated LA and LV, decr. LV function
Tx: Medical and surgical:
Medical: Afterload reduction with vasodilators
Chronic antigoac
Surgical:Mitral valve repair or replacement
67
Valvular heart disease: Tricuspid regurgitation
TR is usually secondary to RV dilation. Other causes: RV-infarction, inferior wall MI.
Tricuspid endocarditis - seen in IV drug users.
Epstein anomaly.
Results from a failure of the tricuspid valve to close completely during systole, causing regurgitation of blood into the RA.
Clinical: Usually asymptomatic unless the pts. develop sx of RHF/pulm HTN
Blowing holosystolic murmur, pulsatile liver
Dx: Echo
Tx: Treat underlying etiology, diuretics for volume overload, treat left sided heart failure, endocarditis.
68
Valvular heart disease: Mitral Valve Prolapse
The presence of excessive or redundant mitral leaflet tissue due to mycomatous degeneration of mitral valve leaflets and/or cordae tendineae. Common in Marfan and Ehler Danlos, osteogenesis imperfecta etc.
Most pts. are asymptomatic for their whole life.
Midsystolic or late systolic click. Mid-to-late systolic murmur.
Dx: Echo
Tx: If chest pain; B-blockers, but unlikely to be required.
69
Rheumatic heart Disease
Occurs as a complication of strep. pharyngitis (group A strep). The most common valvular abnormality is mitral stenosis, but patients may have aortic or tricuspid involvement as well.
```
Diagnosis: Requires two major criteria or one major and two minor:
Major:
Migratory polyarthritis
Erythema marginatum
Cardiac involvement
Chorea
Subcutaneous nodules
```
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Minor:
Fever
Elevated ESR
Polyarthralgias
Prior history of rheumatic fever
Prolonged PR interval
Evidence of preceding strep.infection
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Tx: Treat strep. pharyngitis with penicillin or erythromycin to prevent it. Acute rheumatic fever is treated with NSAIDS. Treat valvular pathology of rheumatic heart disease.
70
Infective endocarditis
Infection of the endocardial surface of the heart (usually involves the cusps of the valves)
Acute:
Most commonly S.aureus
Occurs on a normal heart valve
If untreated, fatal in less than 6 weeks
Subacute:
Caused by Strep.viridans and Enterococcus
Occurs on damaged heart valves
If untreated, takes much longer than 6w to cause death.
S.Viridans is the most common organism in native valve endocarditis, then S.aureus, then S.epidermidis (in prosthetic valve)
In IV-drug users: S.aureus
Dx: Duke clinical criteria: Two major criteria, one major and threeminor criteria or fiveminor criteria are required to diagnose infective endocarditis.
Sjekk om Dukes Criteria
Tx:
Parenteral AB based on culture in 4-6w
If cultures are neg, but high clinical suspicion -> Penicillin or vancomycin + aminoglycoside
71
Hypertensive emergency (General, Causes)
Systolic BP > 220 and/or diastolic BP > 120in addition to end-organ damage - immediate tx is indicated.
Hypertensive urgency = Elevated BP alone without end-organ damage. Lower BP over a period of 24h.
If pts. with markedly elevated BP, check:
a) Eyes: Papilledema
b) CNS - altered mental status or intracranial hemorrhage
c) Hypertensive encephalopathy may develop
d) Kidney failure: renal failure or hematuria
e) Heart: USA, MI, CHF, Pulm edema
f) Lungs: pulm. edema
Hypertensive emergency may lead to post. reversible encephalopathy syndrome (PRES).
Causes: Noncompliance w/antihypertensive drugs
Cushing syndrome, Drugs, hyperaldosteronism, eclampsia, vasculitis, pheochromocytoma
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Hypertensive emergency (Clinical + tx)
Clinical:
Severe headache
Visual disturbances
Altered mentation
Tx:
1. Hypertensive emergencies:
- Reduce mean arterial pressure by 25% in 1-2h
The goal is not to immediately achieve normal BP, but to get the pts out of danger, then reduce BP gradually.
- If severe (diastolic BP > 130), or hypertensive encephalopathy -> IV agents such as hydralazine, esmolol, nitroprusside.
2. Hypertensive urgencies: BP should be lowered within 24h using oral agents.
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Aortic dissection
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Type A (proximal) involves the ascending aorta
Type B (Distal) is limited to the descending aorta
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Predisposing:
- Long-standing HTN
- Cocaine use
- Trauma
- Connective tissue diseases
Clinical:
Severe, tearing/ripping/stabbing pain, abrupt in onset, either in anterior or back of the chest
a) Anterior chest pain more common with proximal dissection
b) Interscapular back pain is more common with distal dissection
Diaphoresis, hypertensive, Pulse or BP asymmetry between limbs
Dx:
CXR: widened mediastinum
TEE has high specificity and sensitivity
Tx: Initiate medical therapy immediately:
- Iv B-blockers to lower heart rate
- IV sodium nitroprusside to lower syst BP
For type A: surgical.
For type B: Medication (lower BP as quickly as possible. First line: IV B-blockers such as labetalol, esmolol.)
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Abdominal Aortic Aneurysm
Abnormal localized dilation of aorta. Most occur between the renal arteries and iliac bifurcation. Risk factors: men over 50 that smokes.
Causes:
- Multifactorial: atherosclerotic weakening of the aortic wall. Orhter predisposing facturs: HTN, vasculitis, smoking and pos. family history.
Clinical:
Usually asymptomatic, often discovered randomly.
Sense of "fullness"
Pain may be present in hypogastrium and lower back. Pulsatile mass. Rupture: sudden onset severe pain in abdomen, back or groin.
Triad of rupture:
Abdominal pain, hypotension, palpable pulsatile abdominal mass.
Dx: USG, CT
Tx: Unruptured: if over 5cm or symptomatic -> surgery.
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Deep Vein Thrombosis
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Cause: Virchow triad (endothelial injury, venous stasis, hypercoagulability) gives rise to venous thrombosis.
RF:
- Age > 60
- Malignancy
- Prior history of DVT
- Hereditary hypercoagulable states
- Prolonged immobilization
- Pregnancy, oral contraceptives
Etc.
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Clinical:
May be subtle
- Lower extremity pain+swelling
- Homans sign (calf pain on ankle dorsiflexion
- Palpable cord
- Fever
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Dx:
Doppler analysis, duplex usg
Venography - most accurate
- D-dimer
Cx:
Pulm. embolus
Postthrombotic syndrome
Phlegmasia cerulea dolens
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Tx:
Anticoagulation
- Heparin bolus followed by a constant infusion and titrated to maintain the PTT at 1,5-2 times aPTT
- Start warfarin once the aPTT is therapeutic, continue for 3-6months
- Anticoagulate to INR 2-3
Thrombolytic therapy
- Streptokinase, urokinase etc
- Speeds up the resolution of clots
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76
Cardiac Neoplasm
Rare. Metastases from other tumors are more common.
Atrial Myxoma:
- Benign growth. Can embolize, leading to metastatic disease.
Sx: fatigue, fever, syncope, palpitation
Tx: Surgical excision
77
Basics of Shock
Underperfusion of tissues. Presents with tachycardia, decrease in BP and malfunction of underperfused orgn systems, most notably:
a) Lactic acidosis
b) Renal (anuria/oliguria)
c) CNS dysfunction (altered mentation)
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Initial approach to a patient in shock
1. Fever + possible site of infection suggest septic shock
2. Trauma, GI bleeding, vomiting, diarrhea suggest hypovolemic shock
3. History of MI, angina or heart disease suggest cardiogenic shock
4. If JVD is present, this suggest cardiogenic shock
5. If spinal cord injury or neurologic deficits are present, neurogenic shock likely.
Initial steps: Simultaneously stabilize pt hemodynamically and determine the cause of shock
- Establish two large-bore venous catheters, a central line, and an arterial line.
- A fluid bolus(multiple liters of normal saline or lactated Ringer)
- Draw blood:CBC, electrolytes, renal function, PT/PTT
- ECG, CXR
- Pulse oximetry
- Vasopressors (dopamine, norepinephrine) if pts remains hypotensive after fluids
79
Cardiogenic shock
Occurs when heart is unable to generate a cardiac output to maintain tissue perfusion.
Can be defined as systolic BP < 90, and urine output < 20 ml/hr.
Causes: After acute MI - most common cause
Cardiac tamponade
Tension pneumothorax
Arrhytmias
Clinical:
Altered sensorium, pale cool skin, hypotension, tachycardia.
Engorged neck veins - Venous pressure is usually elevated.
Pulm. congestion
Dx:
ECG: ST-elevation (common finding)
Echo + hemodynamically Swan-Ganz catheter.
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Tx:
ABC
Treat underlying cause
Vasopressor
Iv fluids are likely to be harmful if left ventricular pressures are elevated. Patients may in fact need diuretics.
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80
Hypovolemic shock
Decr. circulatory blood volume leads to decreased preload and cardiac output. Four "classes" of hypovolemic shock, based on severity of volume loss.
Causes:
a) Hemorrhage
b) Nonhemorrhage
- Bomiting, diarrhea, dehydration, burn, third-space losses.
Dx: Clinical picture, thoguh central venous line can give information for hemodynamic monitoring.
Tx: ABC - generally requireintubation and mechanical ventilation.
Circulation:
a) If hemorrhage is cause, apply direct pressure
b) IV hydration - fluid bolus
c) For nonhemorrhagic shock, blood is not necessary. Crystalloid solution with appropriate electrolyte replacement is adequate.
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Septic shock
Hypotension induced by sepsis that persists despite adequate fluid resuscitation. Results in hypoperfusion and organ system failure. Common causes are pneumonia, pyelonephritis, meningitis, abscess formation, cholangitis, cellulitis and peritonitis.
Clinically, a progression from SIRS, to sepsis, to septic shock to multiorgan failure.
There is a severe decrease in SVR secondary to peripheral vasocilation.
Dx:
Clinically, confirmed by blood cultures, but negative cultures are common.
Tx:
Initially, IV AB broad spectrum at max dosages. Surgical drainage if necessary. Fluid administration to increase mean BP. Vasopressors if hypotension persist.
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Neurogenic shock
Results from a failure of the sympathetic nervous system to maintain adequate vascular tone(sympathetic denervation).
Causes: spinal cord injury, severe head injury, spinal anaesthesia, pharmacologic sympathetic blockade. Characterized by peripheral vasodilation with decr. SVR
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Clinical:
Warm, well perfused skin
Urine output low or normal
Bradycardia and hypotension
Cardiac output decr, SVR low
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Tx:
Judicious use of IV fluids
Vasoconstrictors to restore venous tone
Supine or Trendelenburg position
Maintain body temperature
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