CARDIOLOGY Flashcards
sss
Absolute CVD Risk assessment
Target groups—?
all adults ≥ 45 years without known history of CVD
*ATSIP ≥ 35 years
(Aboriginal and Torres Strait Islander Partnerships)
Aboriginal and Torres Strait Islander Partnerships
Absolute CVD Risk assessment
Specific screening recommendations:
BP?
fasting blood lipids?
diabetes?
kideney disease?
*BP should be measured in all adults from age 18 years at least every 2 years.
*Adults should have their **fasting blood lipids **assessed starting at age 45 years, every 5 years (ATSIP: 35 years).
*Adults should be screened for diabetes(fasting plasma glucose) every 3 years from age 40 years (ATSIP: from 18 years).
*Adults at high risk should be screened for kidney disease every 1–2 years (ACR ratio and eGFR).
Dyslipidemia
Low HDL-C (<1.0 mmol/L) with high triglycerides
first line of therapy in EVERY LEVEL?
NON PHARMACOLOGICAL MEASSURES - life style changes - reacces after 6-8 *weeks
excersice
no smoking
no alcohol
weight reduction
Secondary HTN :
TRACKPADS
TRACKPADS
Thyroid disease (hyper-)
Renovascular disease (renal artery stenosis)
Aorta, coarctation of
Cushing syndrome
Kidney disease, chronic
Pheochromocytoma -headache, sweating, tachycardia
Aldosteronism (hyper-) = Conn’s syndrome -Triad of HTN, unexplained hypokalemia, metabolic alkalosis
Drugs (e.g. OCPs, decongestants, NSAIDS)
Sleep apnoea
Isolated systolic HTN
≥ 140 mmHg in the presence of a diastolic pressure <90 mmHg. Seen in elderly
Refractory hypertension :
BP >140/90 mmHg despite maximum dosage of two drugs for 3–4 month
Classification of HTN
remember to use the high value to classify
Treatment strategy for patients with newly diagnosed HTN
HTN
first line of TX
- Initial monotherapy
Angiotensin-converting enzyme inhibitor
First line management
Drug of choice in CKD with normal GFR
Angiotensin-converting enzyme inhibitor
side effects:
Side effects:
Cough**
**Hyperkalaemia(risk increased by renal impairment)
Renal** impairment (risk increased by hypovolaemia or NSAIDs)
**Angioedema (infrequent; may occur after years of treatment)
second category HTN tx
and side effects
Angiotensinreceptor blocker (Sartans)
*Hyperkalaemia (risk increased by renal impairment)
*Renal impairment (risk increased by hypovolaemia or NSAIDs)
*Cough and angioedema are rare
3th line of treatment side effects
Dihydropyridine (Amlodipine, nifedipine)
*Minimal effect on myocardial contractility and cardiac conduction.
*Do not treat calcium channel blocker induced peripheral oedema with diuretics.
Side effects: Peripheral vasodilation (peripheral oedema, flushing, headache, dizziness), postural hypotension, tachycardia, palpitations, chest pain, gingival hyperplasia
**Nondyhidropyridine(Verapamil, diltiazem)
**
*Less peripheral vasodilation than dihydropyridines.
*Reduce heart rate and depress cardiac contractility (verapamil more than diltiazem).
*Side effects: Bradycardia, constipation (particularly verapamil, may be severe), atrioventricular block, heart failure.
4th tx HTN
Thiazide diuretic:
may be preferred over an ACE inhibitor, ARB, or dihydropyridine calcium channel blocker in patients with:
suggest treating with a thiazide-like diuretic (ie,chlorthalidone,indapamide) rather thanhydrochlorothiazide
edema, osteoporosis, or calcium nephrolithiasis with hypercalciuria
Thiazide diuretic:
side effects:
Side effects: Postural hypotension, dizziness, hypokalaemia, hyponatraemia, hyperuricaemia, hyperglycaemia
HTN TX
5TH LINE
Beta blockers
Side-effects:
Side-effects: Bradycardia, postural hypotension, worsening of heart failure (transient), bronchospasm, cold extremities
HTN TX
5TH LINE
Beta blockers
CONTRAINDICATIONS
severe bradycardia
*preexistingsick sinus syndrome,
*second-and third-degree atrioventricular block
*severe left ventricular dysfunction
*fluid overload
*Ractive peripheral vascular diseasewith restischemia,
*reactive airway diseaseso severe that airway support is required -Asthma
*hypotension
HTN TX IN SPECIFIC POPULATION
BP TX TARGETS
Hypertensive urgency
definition
Hypertensive Crisis
severe HTN (>180/110 mmhg) patients who are not experiencing acute end-organ damage
usually oral HTN with aim to reduce over 24 h
Hypertensive emergency
definition
severe HTN (>220 /> 140 mmHg) with evidence of acute end-organ damage
Chest pain (ischemia/MI), Back pain (aortic dissection), Altered mental status (encaphalopathy), renal disease
Hypertensive emergency
TX
Life-threatening and require immediate treatment, usually with parenteral medications (labetalol, nitroprusside, nicardipine) in a monitored setting
Aim to reduce the BP by no more than 25% within the first 2 hours to prevent cerebral hypoperfusion or coronary insufficiency -> then towards 160/100 mmHg within 2 to 6 hours.
Malignant HTN
definition
DBP> 120 mmHG and exudative vasculopathy in the retinal and kidney circulations
renal artery stenosis HTN
age and etiology
Common in patients <25yrs and >50yrs with recent onset HTN
**Fibromuscular dysplasia **in younger pts
atherosclerosis (MCC) in older pts
renal artery stenosis
MX
Initial inv for **stable cases **-Doppler Duplex USG
*Initial inv for unstablecases -CT angio
renal artery stenosis
TX
Start 1stline ACE inhib/ARB
2ndline CCB
Percutaneous renal artery angioplasty for recurrence/refractory/PE
*Reduce hypercholesterolemia with Statins
*Diuretics NOT recommended
- ACEI is considered in unilateral cases. In bilateral cases, ACEIs can accelerate kidney failure by preferential vasodilation of the efferent arteriole
Pheochromocytoma
Symptoms
Episodic headache, sweating/diaphoresis, palpitations/paroxysmal tachycardia
Pheochromocytoma
investigation of choice
BEST = 24hr urinary metanephrines and catecholamine levels
or
Plasma metanephrines
Pheochromocytoma
TX
First give Alpha blockers to control HTN
*Next give BB to control tachycardia. (never give BB first as unopposed alpha-adrenergic stimulation will lead to refractory HTN)
refractory=
*Surgical resection
Conn’s Syndrome/Hyperaldosteronism
Diagnosis TRIAD
Excessive secretion of aldosterone from zona glomerulosa of adrenal cortex.
HTN,
unexplained hypokalemia,
metabolic alkalosis
Mild hypernatremia
*Hypomagnesemia
*Inc Plasma aldosterone, Dec Renin level and Inc aldosterone/renin ratio
coronary artery disease 4 types: flow chart
Angina Pectoris (Stable Angina)
definition
Retrosternal chest discomfort (pain or tightness) that lasts **10 minutes **or less and subsides promptly with rest.
it occurs when myocardial oxygen demand exceeds supply, which is usually restricted by athero
most common are shortness of breath, nausea, and diaphoresis
Angina Pectoris (Stable Angina)
mx
ST segment changes on exercise stress test with ECG monitoring*
Troponin -They are unlikely to be elevated in patients with intermittent and relatively brief angina episodes. However, they may be useful when the anginal episode is more prolonged and for prognostication
Prinzmetal Angina
definition
popultation
Prinzmetal’s (variant) angina mimics angina pectoris but is caused by vasospasm of coronary vessels.
It classically effects young women at rest in the early morning and is associated with ST-segment elevation in the absence of cardiac enzyme elevation.
The typical patient is a female smoker
Prinzmetal Angina
vs
angina estable
activity:
symptoms:
akg and no symptoms”:
ekg and symptoms:
cath findings:
treatment:
Prinzmetal Angina
TX
These episodes tend to self-resolve; however, cardiac-selective calcium channel blockers such as verapamil or diltiazem
CARDIAC SELECTIVE
NIFEDIPINE
Angina Pectoris
Tx for Episodes of Angina:
Glyceryl trinitrate
Before taking glyceryl trinitrate, they should sit down, to avoid orthos
Glyceryl trinitrate spray 400 micrograms sublingually, repeat every 5 minutes if pain persists, up to a total of 3 doses if tolerated angina, treatmentORGlyceryl trinitrate tablet 300 to 600 micrograms sublingually, repeat every 5 minutes if pain persists, up to a total of 3 doses if tolerated.
Action plan for pre-hospital angina:
**Rest + nitrate
*Aspirinif no CI
*call ambulance if pain doesn’t subside in 10 min**
Angina Pectoris TX Prevention of Angina:
Combo of 2 antianginal drugs
- ***Short-acting glyceryl trinitrate **can be taken before exercise that is likely to provoke angina
- *Beta blockers(atenolol, metoprolol tartare) enhance exercise tolerance by reducing myocardial oxygen demand. In LV dysfunction use these BB instead Carvedilol, bisoprolol, nebivolol or metoprolol succinate
- Nondihydropyridine CCB (diltiazem, verapamil) reduce heart rate and can be used as an alternative if beta-blocker therapy is contraindicatedor not tolerated
Do not use BB and diltiazem/Verapamil NOT = severe bradycardia and heart failure!!!
. *Avoidusing diltiazem or verapamil for patients with left ventricular dysfunction (LVEF <40%)
- dihydropyridine calcium channel blocker(amlodipine, modified-release nifedipine) can be added to a beta blocker if angina persists
- **Long-acting nitrate **(transdermal glyceryl trinitrate, modified-release isosorbide mononitrate) can be added either to a beta blocker, or to a nondihydropyridinecalcium channel blocker (diltiazem, verapamil)
- Nicorandilis an option for patients with refractory angina despite optimal therapy with the preceding drugs. Add to beta-blocker, diltiazem or verapamil therapy
atenolol 25 mg orally, daily, increasing if required up to 100 mg daily
OR
metoprolol tartrate 25 mg orally, twice daily, increasing if required up to 100 mg twice daily
ACUTE CORONARY SYNDROME
Typical presentation
Typical presentation
crushing or heavy central chest pain that may radiate to the arms, neck, back and jaw. Left arm pain is common, but bilateral or right arm pain are more specific.
An acute coronary syndrome may be associated with shortness of breath, nausea and sweating
ACUTE CORONARY SYNDROME
Atypical presentation
*burning pain, pain that increases with respiration, sharp pain (patients sometimes say ‘sharp’ when they mean ‘severe’ pain)
*upper abdominal pain.
Pain may also be absent (‘silent’ acute myocardial infarction). In particular, consider an acute coronary syndrome in patients with *diabetes and older patients who have no pain but do have associated symptoms (egshortness of breath, nausea, sweating), or poorly controlled diabetes.
ACUTE CORONARY SYNDROME
When to suspect ACS:
Rest angina, which is usually more than 20 minutes in duration
*New onset angina that markedly limits physical activity
*Increasing angina that is more frequent, longer in duration, or occurs with less exertion than previous angina
Acute coronary syndromes result from unstable atherosclerotic plaques or endothelial disruption, with associated transient or permanent thrombotic occlusion of the coronary arteries, leading to myocardial infarction and ischaemia
Classification based on ST elevation
**1. ST elevation myocardial infarction (STEMI)—a medical emergency
*According to guidelines, to diagnose Acute STEMI. Patient should have chest pain/discomfort suggestive of AMI in the presence of ST elevation more than 1mm in two contagious leads , or a newly developed LBBB.
- Non–ST elevation acute coronary syndrome (NSTEACS)—the initial description for patients without ST elevation. Subsequent investigation divides NSTEACS into:
** A)** Non–ST elevation myocardial infarction (NSTEMI)—patients with MI as determined by elevated cardiac biomarkers
** B)**Unstable angina—patients without elevated cardiac biomarkers. It signals impending infarction.
NSTEACS can progress to STEMI; ongoing monitoring is essential
Universal classification of MI
Type 1 spontaneous MI -atherothrombotic coronary occlusion
Type 2 MI -is secondary to ischaemic imbalance
tachyarrhythmias, bradyarrhythmias, anaemia, respiratory failure and hypotension
assesmment INV of acute chest pain
- ECG -12 leads WITHIN 10 MIN of arrival to ER
normal does not rule out IM -
TROPONINE
**Repeat Troponin levels after every 3-4hrs
OTHER CAUSES OF TROPONIN ELEVATION
ECG leads & area of STEMI
Mx during initial assessment
Mx of confirmed STEMI
A) Percutaneous coronary intervention
or
B)fibrinolytic therapy.
Consider all patients with a STEMI for admission to a coronary care unit for monitoring and expert acute care
Started within the 12 hours preceding presentation
Mx meds in confirmed STEMI
Dual antiplatelet therapy for STEMI -
1) with aspirin
2) P2Y12 inhibitor (clopidogrel, prasugrel, ticagrelor)
For a patient receiving fibrinolytic therapy, give with aspirin CLOPIDOGREL!
Reperfusion therapy
time?
PCI is available within 90 minutes of first medical contact, PCI is preferred over fibrinolytic therapy.
2.If PCI cannot be delivered promptly, fibrinolytic therapy should be given within 30 minutes of the patient arriving at the hospital.
.3 PCI is not available, and fibrinolytic therapy is not an option for them, then** promptly transfer them to a centrewhere PCI is available**.
In some healthcare services, paramedics can give fibrinolytic therapy before the patient reaches hospital
Percutaneous coronary intervention
(transluminal coronary balloon angioplasty and stenting)
complication + tx
nsignificant CAD is defined as stenosis <50% and does not often require intervention.*Significant stenosis
**(>50%) may be considered for ballooning, atherectomy, stenting****
Psuedoaneurysmat the site of insertion is a complication of PCI. It is a haematoma with communication to the artery (iliac/femoral/peroneal) that appears as a pulsatile painful mass in groin. It is treated by USG guided thrombin injection away from the neck of sac
PIC
adjuvant medication
Adjuvant drug therapy:*
dual antiplatelet therapy—aspirin + P2Y12 inhibitor
*periprocedural anticoagulation:—UFH, enoxaparin or bivalirudin.
**glycoprotein IIb/IIIa inhibitor may also be indicated.
Fibrinolytic therapy :
meds
aboriginals?
complications
Alteplase OR Reteplase OR Tenecteplase
Aboriginal Australians have high prevalence of IgG anti-streptokinase Ab, making Streptokinase inappropriate for thrombolytic therapy
1) should also be given a parenteral anticoagulant (enoxaparin or UFH). Bleeding can occur following treatment with a fibrinolytic drug and a parenteral anticoagulant.
2) .Significant arrhythmias including ventricular fibrillation can occur after reperfusion with fibrinolytic therapy.
Fibrinolytic therapy-CI
Absolute contraindications
- any prior intracranial haemorrhageknown structural cerebral vascular lesion (egAV malformation)
- *known malignant intracranial neoplasm (primary or metastatic)
- *ischaemic stroke within 3 months, except acute ischaemic stroke within 4.5 hours
- *suspected aortic dissection
- *active bleeding or bleeding diathesis (excluding menses)
- *significant closed head or facial trauma within 3 months
NSTEACS -Management
antiplatelet therapy and consider treatment with parenteral anticoagulant therapy, beta-blocker therapy, glycoprotein IIb/IIIa inhibitors and invasive management.
*Fibrinolytic therapy is NOT used to treat NSTEACS
Clinical trials have demonstrated the benefit of early invasive management for NSTEACS -coronary angiography and revascularisation[iestenting or bypass surgery]).
very high risk—recommended within 2 hours of admissionhigh risk—recommended within 24 hours of admission*intermediate risk—recommended within 72 hours of admission
Long-term management of ACS
antiplatelet therapy,
a statin,
*a beta blocker
*an ACEI.
*~Oral anticoagulation may be needed for patients with complications associated with myocardial infarction, such as mural thrombus or atrial fibrillation.
Dual antiplatelet therapyAspirin (75-150 mg) + a P2Y12 inhibitor[clopidogrel, prasugrel, ticagrelor])
For patients who have had a coronary stent inserted, dual antiplatelet therapy is** usually recommended for 12 months after an ACS**.Dual antiplatelet therapy for less than 12 months may be appropriate for patients at high risk of bleeding, and longer than 12 months may be appropriate for selected patients at high risk of recurrent ischaemicevents.When stopping dual antiplatelet therapy, stop the P2Y12 inhibitor and continue aspirin indefinitely.If aspirin is contraindicated, consider indefinite therapy with a P2Y12 inhibitor alone.
DAPT and surgery
months. of therapy
at least 6 weeks (ideally 3 months) following angioplasty with BMS
12 months after DES,
Post MI complications
1stday: V.Fibanytime within 24hrs and especially within 1hr and Heart failure
*2-4 days: **
*Arrythmia -Most** common
*Pericarditis -when occurring post MI, Aspirinis the treatment of choice and not other NSAID
*5-10 days:
*LV wall rupture (acute pericardial tamponade)
*Papillary muscle rupture with severe MR
Weeks to months**:
**Dressler’s syndrome occurs 2 -10 weeks post MI -autoimmune process with fever, pericarditis, pleural effusion, leucocutosis, incESR. Rx of choice is Aspirin if the cause is post MI.
*CHF, arrythmia, persistantST elevation, MR, thrombus formation
most common arrhythmia in the course of MI ?>
Ventricular tachicardia
Classification of CHF
Heart failure with reduced ejection fraction (HFrEF
LVEF <50%
Impaired ventricular contraction
Heart failure with preserved ejection fraction (HFpEF)
LVEF >50%
impairment of left ventricular filling
Diastolic CHF definition
and basic tx
Impairment of left ventricular filling with preserved systolic function
inotropic agents such as calcium-channel blockers (verapamil or diltiazem) and beta blockers.
If possible, avoid diuretics (except for congestion), digoxin, nitrates/vasodilators and nifedipine. Excessive diuresis from overzealous diuretic therapy can cause severe consequences for cardiac output. ACE inhibitors can be used with caution.
Systolic CHF most important cause?
IHD
CHF: = Symptom most common
signs
prognosis
EXERTIONAL DYSPNEA earliest and most common symptom
Prognosis of systolic HF can be predicted by JVP and S3 sound. Elevated JVP and presence of S3 indicates poor prognosis.
CHF: Pathophysiology
CHF
investigation
INITIAL
+
DIAGNOSTIC
1.CXR - cardiomegalia, pulmonary vesels etc
ECG not diagnostic but can help found out the cause.
DIAGNOSTIC
- echocardiograma EF <50% and ventricular dilatation **
B-type Natriuretic peptide >400
**if the diagnosis is unclear and an echocardiogram cannot be arranged in a timely fashion, then measurement of plasma B-type natriuretic peptide (BNP) or N-terminal pro-BNP levels improves diagnostic accuracy. It is highly sensitive although less specific for active CHF)*
The New York Heart Association (NYHA) functional classification
Mx of CHF
initial therapy
- includes a combination of diuretic therapy (as need to treat volume overload),
- an angiotensin system blocker (ACE inhibitor, or single agent ARB),
- beta blocker
In patients with a decompensated heart failure which was previously controlled :
initial assessment of volume status.
1.If hypervolemic -First step is volume reduction using loop diuretic such as furosemide, bumetanide or torsemide. It is also important to start patient with ACEIs (or ARBs IF ACEIS is not tolerated).
2.If euvolemic -an ACEI (or ARB) + a BB is the management of choice.Aldosterone antagonist (Spironolactopne) is used in euvolemic pts who have GFR >30ml/min and serum K level of <5mmol/lit with close monitoring of potassium levels
3.When euvolemic after hypervolemic -add a cardio selective BB
*** BB should only be started in pts who do NOT have crackles and no more than minimal peripheral edema. ~ BB is contraindicated in volume overload
**Digoxinis indicated with EF <35%. It should be added only after maximally tolerated dose of BB. It is also the initial management of pts with AF and decompensated HF
**
Hypervolemic state:
Inc JVP
*Inc weight
*Dyspnea
*Crackles
*More than minimal peripheral edema
*Elevated BNP
*Hepatomegaly, ascites or anasarca in severe cases
Acute pulmonary edema/congestion
symptoms
inv
Tx:
s/s : dyspnea, bibasal coarse crackles
investigation: CXR
TX: LMNOP
-Lasix -IV furosemide is one of the the initial step.
Morphine** -decreases sympathetic tone causes vasodilation and reduction of preload
**Nitrates-GTN reduces preload
Oxygen** -cannula, Hudson mask; CPAP, BiPAP for reducing venous return and preload
**Position( upright)
Hypertrophic cardiomyopathy
Causes:
*HTN
Aortic stenosis
HOCM
*O/E: *S4 gallop, Systolic murmur of MRSystolic murmur radiating to axilla due to LVTO
*Initial inv: *CXR -left atrial enlargement secondary to mitral regurgitation
*ECG (signs of LVH)
*Diagnostic inv : Echo-shows asymmetrical thickened septum, dynamic obstruction of blood flow, valvular lesions
Hypertrophic obstructive cardiomyopathy (HOCM)
TREATMENT
*is a congenital form, inheritedas an autosomal dominant train in 50% of HOCM pts.
Significant cause of sudden cardiac death in young people, including athletes.
**Positive family history **for sudden death at young age.
*Sudden loss of consciousnessin a young person while on exertion is most likely due to arrhythmia or HOCM
-
INITIAL=
BETABLOCKERS
CCB = DILTIAZEM / VERAPAMILO
->
implantable defibrilator if there is syncope
surgery severe cases-septoplastia
AVOID DIGITALIS, DIURETICS, VASODILATORS, EXCERSICE!
Bradyarrhythmias when TX?
Bradyarrhythmias should only be treated if they are causing significant haemodynamiccompromise
bradycardia TX is when is due to SA node dysfunction or AV node level block:
Atropine is the most effective treatment.
*If atropine is ineffective, consider transcutaneous or temporary transvenous pacing.
*If pacing is delayed or not immediately available, consider using chronotropic drugs (egisoprenaline, adrenaline).
*Use with caution because they can provoke serious ventricular arrhythmias.
*Adrenaline is preferred if systolic blood pressure is very low(less than 80 mmHg) because isoprenaline may further reduce blood pressure
dosis
.Atropine 0.5 mg IV, repeat after 3-5 minif necessary, uptomax of 3 mg.Adrenaline (epinephrine) 2 to 10 micrograms/minute by intravenous infusionIsoprenaline2 to 10 micrograms/minute by intravenous infusion
bradycardia due to AV block complicating acute myocardial infarction TX:
eperfusion therapy with urgent PCI
AV block in inferior myocardial infarcts block an tx?
.
AV block in anterior myocardial infarcts tx?
block is usually at the **level of the AV nodeand **is transientand not haemodynamically significant. Atropine may be required
AV block is at the level of the distal conducting tissues in the ventricle and is likely to be permanent and associated with haemodynamiccompromise. Emergency temporary pacing is usually required
Sinus Bradycardia TX
*None if asymptomatic
*Atropinewill incHR
*Pacemakerin severe
First degree AV block
definition
tx
Regularly Long PR interval
*PR interval > 200ms ( >5 small squares).
Age related degeneration of AV Node -MCC
No specific treatment is required. Is symptomatic use Atropine
Second degree Type I (Mobitz I/Wenckebach)
defintion
tx
longer, longer, longer, DROP, now you have a Wenckebach.”
*Progressively longer PR intervaltill one blocked/missed beat.
AV nodal blocking drugs (BB, CCB, Digoxin, amiodarone)
Increased vagal tone, Athletic trainingInferior MI
Myocarditis
S/S: Usually benign, asymptomatic, low risk of progression to 3rddegree heart block
TX:Usually no Rx needed. Atropine if symptomatic. **Remove triggers*
Second degree Type II (Mobitz II)
Intermittent non-conducted P waves without progressive prolongation of the PR interval
Anterior MI, *Fibrotic disease of conducting syste
S/S: Likely to have haemodynamic compromise and progression to 3rddegree heart block
Tx: PACEMAKER (transcutaneous or transvenous) ** Tx MI
Third degree (Complete) AV block
Severe bradycardia due to absence of AV conduction
*Complete AV dissociation,
S/S: Syncope (if self-terminating) or sudden cardiac death (if prolonged)*Rx: PACEMAKER
Sick Sinus Syndrome
important in australia
Sinus node dysfunction (formerly called sick sinus syndrome)
*Aka Tachycardia-bradycardia syndrome
intrinsic causes: idiopathic degenerative fibrosis (most common
extrinsic: meds
Chronic sinus node dysfunction associated with symptoms is an indication for permanent pacing but rarely requires acute intervention.
*It is a leading reason for a cardiac pacemaker (in Australia it accounts for approximately 46% of devices
Sinus Tachycardia
SUPRAVENTRICULAR TACHYARRHYTHMIA
This is usually benign
*Anxiety or stress, Response to fear, pain, exercise.
*Less often -thyrotoxicosis,anaemia, infection, pulmonary embolism.
*S/S: palpitations, SOB, HR 100 -150 bpm
Atrial Fibrillation *****
defintiion
Presents with irregular ventricular rate of about 160–180 beats/minute in untreated patients with a normal AV node. absence of distinct P waves
Atrial Fibrillation
ACUTE AF
CHRONIC AF
etiology
ACUTE = PIRATES
-Pulmonary disease
-Ischemia
-RHD
Anemia
Thyrotoxicosis
Ethanol, electrolyte abn
Sepsis
chronic HTN most common cause of AF
CHF
Atrial Fibrillation
Potentially reversible precipitants:
*Hyperthyroidism
*Alcohol excess
*Electrolyte abnormalities
*Sepsis
AF TX RATE CONTROL
1 line
2 line
3 line
4 line
- Lastly, consider pacemaker insertion followed by atrioventricular (AV) node ablation.
*Best used for patients who have failed treatment with pharmacologicagents or cannot tolerate them due to hypotension
AF TX RYTHM CONTROL
WHO:
it can be helpful in patients who remain symptomatic despite adequate rate control therapy.
are physically active
*have paroxysmal or persistent AF lasting short periods of time
*do not have significant underlying cardiac structural changes
AF TX RYTHM CONTROL:
electrical cardioversion or antiarrhythmic drugs like
For both methods of cardioversion, assess the stroke risk. Use CHA2DS2-VASc score!
Immediately start anticoagulant therapy with UFH or LMWH in men with a score of ≥ 1 or women with a score of ≥ 2whoare to undergo cardioversion
FLECAINIDE
SOTALOL (renal)
AMIODORONE (liver - pulmonary fibrosis)
AF TX :
anticoagulation indications :
Higher risk of embolism in AF >48hrs because left atrial thrombi likely to form due to atrial stagnation:
1.those in whom cardioversionto sinus rhythm is being considered (regardless of the CHA2DS2-VASc score or method of cardioversion [electrical or pharmacologic]).
2.those who meet criteria for long-term anticoagulation (risk of embolization exceeds the risk of bleeding)
In all pts with AF, assessment should be done prevent systemic embolization even for the first AF episode.Use** CHA2DS2-VASc score**
*Risk of bleeding is assessed through HAS-BLED score
*In planned cardioversion, anticoagulation should be started 3-4 weeks before to 4 weeks after
CHA2DS2-VASc score for AF Stroke risk
AF TX :
ANTICOGULATION MEDS>
NOAC-indicated in non-valvular AF only. Do not use in pts with renal impairement.
*Warfarin-In the special case of ‘valvular AF’ (defined as the presence of a mechanical heart valve or moderate-to-severe mitral stenosis),warfarin therapy is the only effective recommended treatment option, and the NOACs should not be used.It is also used in non-valvular AF.
*Heparinis used with warfarin initially till the INR levels fall within 2-3 and then warfarin only
AF Mx Plan
Pte. Haemodynamically Unstable:
Immediate electrical cardioversion synchronized with sedation (emergency)
AF Mx Plan
Hemodynamically Stable and AF lasting >48hrs
Rate or rhythm control strategy may be considered
Rate control is the preferred initial treatment (if thrombus cannot be excluded or ptnot on anticoag)
Defer acute cardioversion unless left atrial thrombus has been excluded, or the patient has had therapeutic anticoagulation for the previous 3 weeks.
*Transoesophagealechocardiography (TOE) may be considered to exclude left atrial thrombus and allow early cardioversion. For these patients, anticoagulant therapy should be started at the time of cardioversion and continued for a minimum of 4 weeks after cardioversion
1.- beta
2.block Channels C
Atrial Flutter
definition
**Narrow complex tachycardia
**
*Regular atrial activity at ~300 bpm
ventricular rate 125-150
*Loss of the isoelectric baseline
*“Saw-tooth” pattern of inverted flutter waves in leads II, III, aVF
Atrial flutter commonly reverts with a low-energy direct current (DC) shock
treatmen similar to AF (insensive to antiarrhythmic drug therapy
difference to atrial fibrilation by the irregular rhythm
Supraventricular Tachycardia
def
tx
Sudden-onset regular rapid palpitations will signify episodes of SVT . HT 150-200
younger patients like athletes,
STABLE
- 1 first LINE vagal manoeuvres (valsava , cold stimulus face, carotid massage (avoid in older pts and those with vascular disease)
-
- 2n LINE if vagal doesnt work
- **ADENOSINE IV
- VERAPAMILO IV
- METROPROLOL IV (no in asthma)**
-3 LINE CARDIOVERSION
UNSTABLE
Cardioversion !
AV Reentrant Tachycardia (AVRT)
def
tx
ectopic connection between atria and ventricle that causes a reentry circuit
WPW syndrome
Short PR interval -coz of preexcitedVentricular tissue
*Delta wave -V stimulation for a longer period of tim
Tx
stable - vagal meassures, antiarrythmics
unstable - DC cardioversion
AV Nodal Reentry Tachycardia (AVNRT)
A reentry circuit in AV node depolarizes atrium and ventricle simultaneousl
ECG: rate 150-250 bpm
S/S: Palp, SOB, angina, syncope, lightheadedness
Tx
stable - vagal meassures, antiarrythmics
unstable - DC cardioversion
Ventricular ectopic beats
Ventricular rhythms: No P wave, Wide QRS
inv
tx
Hypoxia, electrolyte imbalance, hyperthyroidism
Inv: *ECG-early wide QRS( >440 msec, ~ 11 small boxes), not preceded by a P wave
Rx:*Treat underlying cause
*If symptomatic:
1stline is BB (atenolol, metoprolol), 2ndline Verapamil or flecainide
if AUSENCE OF HEART DISEASE OR SIGNIFICANT RISK FACTORS REASURANCE
Ventricular Tachycardia (VT)
DEF
types
VT is 3 or more ventricular ectopic beats at a rate of > 130 beats/min
ustained VT is if it lasts > 30 seconds
Monomorphic (MC) -regular, wide (≥120 milliseconds) QRS complex tachycardia with uniform and stable QRS morphology
Polymorphic -multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration
Ventricular Tachycardia (VT)
etiology
ECG
Etiology:*MCC is CAD, MI
ECG: 3 or more VEB, Wide QRS complexes
Ventricular Tachycardia (VT)
TX
Sustained VT Rx
1.-UNSTABLE
check for pulse
A) PULSLESS VT: is a shockable rhythm. So CPR + Defibrillation (unsynchronous cardioversion)
B) WITH PULSE: Non-shockable rhythm. So Synchronized Cardioversion
2.-STABLE*antiarrhythmic drug therapy
-Amiodarone is 1stline
——————————
NON Sustained VT Rx
1stline: BB-Atenolol, metoprolol
2ndline**: **Verapamil** or **flecainide** may be a suitable alternative if beta blockers are contraindicated or not tolerated, provided the patient has no evidence of left ventricular dysfunction. Also avoid flecainide if the patient has coronary disease.
**3rdline: If symptoms persist or there is suspicion of a cardiomyopathy secondary to the nonsustained ventricular tachycardia consider amiodarone
*4thline: Consider catheter ablation for a patient with significant symptoms not controlled by drug therapy, or if there is suspicion of cardiomyopath
IN CHILDREN WITH WIDE QRS ASYMPTOMATIC OR STABLE ( SUSTAINED OR NOT if has symptoms) = **ADENOSINA **
Porque en ninos un QRS ancho > 0,09 sec = puede ser SVT with aberrancy, en adultos es mas del ventriculo.
metabolic Causes of QT prolongation
QT>0,45
Hypocalcemia, hypokalemia, hypomagnesemia
Causes of QT prolongation meds
QT NORMAL <0,44S
PROLONGADO>0,44
Antiarrhythmic-Sotalol, amiodarone, flacainamide
Antipsychotics**-haloperidol, chlorpromazine
**SSRI, TCA
Antihistamine**
**Antifungal -ketoconazole, fluconazole
*Abx -Azithro, erythro
*Antimalarial -chloroquine
*Domperidone
*Opiate -methadone
*Other -arsenic, droperidol
Ventricular Fibrillation ekg
Chaotic irregular deflections of varying amplitude
*No identifiable P waves, QRS complexes, or T waves
*Rate 150 to 500 per minute
**Torsades de pointes
**
Type of polymorphic VT in which the QRS axis constantly shifts
TX?
S/S frequently self limiting
Treatment involves immediately stopping any drug suspected of causing TdP, and correcting electrolyte abnormalities.
*Drug-induced TdPand to control underlying bradycardia: **IV Magnesium Sulphate **or IV Isoprenaline or temporary transvenous pacing
*Congenital QT prolongation: Metoprolol, propranolol. Consider implantable cardioverter defibrillator.
*If TdPhas an underlying bradycardia: Use Atropine
Ventricular Fibrillation ekg
TX
*ACLS protocol
*Immediate electrical cardioversion
syncope
Systolic Murmur: (after S1)
Aortic Stenosis, Pulmonary Stenosis
*Mitral Regurgitation, Tricuspid regurgitation
*Mitral valve prolapse
Diastolic Murmur: (after S2
Aortic Regurgitation, Pulmonary regurgitation
*Mitral stenosis, Tricuspid stenosis
Aortic stenosis
ss
dx
rx
Most often in elderly–heard at the apex
Ejection systolic murmur, that radiates to the carotids.
in elderly to the apex
most comon dyspnea
syncope
dx: ECHO TTE
TX:
Aortic valve replacementespif aortic area <0.7 cm2
*Furosemide for symptomatic relief initially
*Metoprolol for angina
Aortic Regurgitation
etiology
ss
dx
tx
Chronic –Calcified aortic sclerosis,
dilatation of ascending aorta from HTN, Connective tissue disorder (Marfan’s syndrome
Acute –Aortic dissection, infective endocarditis, RF, chest injury
-Increased pulse pressure –high SBP due to incstroke volume and low DBP
Corrigan**’s pulse (bounding carotid pulse), Water hammer pulse (radial and ulnar artery)–rapid systolic rise and rapid diastolic collapse
De **Musset**’s sign –head bobbing synchronous with heartbeat
**Decrescendo early-Diastolic blowing murmur at the lower left sternal borde**
**Systolic flow murmur at Aortic area/Apex –due to inc blood flow across aortic valve
*Austin-Flint murmur low pitched mid-diastolicrumble at apex –due to a functional MS -severe AR
dx - echo
tx Vasodilators/ACEI, Aortic valve replacement
Mitral Stenosis
mcc is?
reumatic fever
Mitral Stenosis
murmur
tx
predominant in young
Opening Snap ->Mid-diastolic murmurat Mitral area (rapid filling phase)
tx
BB/diuretics/ Antiarrhythmics and anticoagulants as AF is common
*Percutaneous balloon valvuloplasty –in favorable valve morphology
*Mitral valve replacement
Mitral Regurgitation
etiology
signs
dx
tx
Etiology -
*Primary: affecting mitral leaflets (MVP, ruptured chordae tendineae, calcific degeneration)
*Secondary ischemic: Reversible ischemia or papillary muscle infarction (AMI)
*Secondary non-ischemic: RF, Papillary muscle apical displacement (LVH)
*Signs –Holosystolic/Pansystolic murmur (flat, no change in intensity) in Mitral area, radiating to axilla
*Diag–Echo, Angiography (assess severity)
Tx –Vasodilators (ACEI/ARB)/Antiarrhythmics as AF is common*Valve repair vs replacement
papilary muscle disfuction vs infarction (EF %< 50
rupture)
Mitral valve prolapse
etiology
signs
females more than males
Primary –Sporadic, familial (AD, XR)
*Secondary –Connective tissue disorders, cong. disorder
signs
Mid-systolic non-ejection click followed by Systolic Murmer
summary valvular
Aortic Aneurysm
def
risk factors
Dilatation greater than 1.5 times the expected diameter of all three layers of the aortic wall
An infrarenal aorta 3 cm in diameter or more OR having increase >50% from baselineis considered aneurysmal
Advancing Age -rarely seen <50
*M > F
*Family history of aortic dissection or thoracic aortic aneurysm –20% risk of AAA
*Atherosclerosis–eg: Smoking, HTN, hypercholesterolemia
*Other vascular aneurysm
*Prior aortic dissection
*Marfan’s, vascular Ehlers-Danlos, Turner, or other connective tissue disease.
*Known aortic valve disease (eg, bicuspid aortic valve, aortic valve replacement, or aortic stenosis).
Usually asymptomatic, incidental finding
*AAA -Epigastric pain radiating to back
Thromboembolism
Signs: Pulsatile abdominal mass, abdominal bruit
Dx: USG (bedside –FAST)
CT abdwith contrast & MRIin elective settings, if diagnosis uncertain and ptis stable*CT angiogram
Aortic Aneurysm
screning n surveillance:
surgical repair
Ruptured Aortic Aneurysm
triad
inv
ct sign
mx
Classic triad’–*
Pain -severe tearing abdominal pain radiating to the back
*Hypotension/circulatory compromise
*Pulsatile mass in abdomen
Inv: *USG/FAST
*CT –Crescent signacute haematoma within the thrombus or wall *sign of impending rupture or contained rupture
*Mx: Immediate FAST USG -> DRSABC -> emergency surgery
retroperitoneal savable / peritoneo muertisimo
Pseudoaneurysm
def
etiology
ss
dx
TX
Haematoma that forms as a result of leaking hole in an artery. Haematoma MUST communicate to the arteryto consider it pseudoaneurysm. Haematoma forms outside the wall and is contained by the fibromuscular tissue
femoral
Trauma, iatrogenic injury(at the anastomotic site of sx) or infection
Asymptomatic pulsating mass, Painful pulsating mass with associated hematoma +/-bruit
Doppler Duplex USG
TX
**USG guided thrombin injection away from the neck of sac **-Femoral/Iliac/peroneal
*Angiographic interventionretrograde approach –for acute vessel occlusion due to distal emboli
Aortic Dissection
most common secundary to HTN
ss?
dx?
Separation of the layers of the aortic wall due to a transverse intimal tear
Tear in intima ->blood enter media ->creates false lumen ->haematoma that propagates longitudinally
Symptoms: chest pain anteriorly (ascending aorta); radiating to back(descending aorta)
Typically, Hypertensive with compensatory tachycardia.
*Asymmetric pulses and BP measurements
*Murmur of AR –if aortic valve involved
*STEMI
*If hypotensive –consider pericardial tamponade,
DX
Transesophageal echo -1stchoice –provides details of artery, pericardial effusion, AR, MI
Aortic Dissection
MX
Ascending aortic dissection–are surgical emergencies
*Descending aortic dissection –emergencies that can be often treated medically
*Meds: Monitor and manage BP and HR –Start B Blockers before starting vasodilators
Morphine -> B Blockers -> Arrange TEE (or CT angioif TEE not available) -> Surg/Med
*Absolute CONTRAINDICATION! -Aspirin, clopidogrel, anticoagulants, and Thrombolytics
Peripheral Arterial Disease
Atherosclerotic disease, causing restriction of blood flow .
Predominantly due to progressive luminal narrowing (stenosis/occlusion) althought a trombosis can occur.
asymtomatic
risk factors: smoking
hx CVD
HTN
diabetes
Peripheral Arterial Disease PAD
location of stenenosis
Aortoiliac disease: **
*Affects Common Iliac artery, External iliac artery
*Pain in buttocks, especially when walking up the stairs
Decreased femoral pulses
**Male impotence -Leriche’s syndrome
***Femoropopliteal disease:
** *Affects most commonly superficial femoral artery
*Pain in calf
*Decreased pulses below the femoral artery Subtotal occlusion of Rt CIASFA stenosis
Peripheral Arterial Disease PAD
DX
MX
*1stline Duplex USG-assess flow, stenosis >75% is clinically significant
*2ndline CT angiography –done before intervention/operative planning.
*Digital Subtraction angiography, MRA
TREATMENT:
SM –Avoid smoking, eat healthy, exercisecan develop collateral circulation*Meds –Anti HTN, lipid-lowering agents, glycemiccontrol
*Cilostazol (phosphodiesterase III inhibitor)–good for intermittent claudication pain
*Antiplatelet (aspirin, clopidogrel) –especially after surgery
*Surgical intervention -endovascular angioplasty or stenting, peripheral bypass or endarterectomy
Reperfusion injury
mx
Paradoxical exacerbation of cellular dysfunction and death, following restoration of blood flow to previously ischaemic tissues
Tx:
*Supportive
*NSAIDS for pain
*compression stockings for edema
Acute Limb Ischemia
6 ps
mx
sudden occlusion
most common site: ?
Commonest site: Common femoral artery
6 P’s of Acute Ischemia:
*PAIN –sever and sudden
*PALLOR
*PARALYSIS(light touch, weakness)–Most reliable indicator for immediate SURGERY
*PULSE DEFICIT
*PARASTHESIA
*POIKILOTHERMIA –least reliable
reversible within 4hrs of symptoms with intervention.
*Diagnosis: Usually enough by history and physical examination
1stline investigation is CT angiography** -Done before interventions, as it can give a lot of info
+
. **Antithrombotic: IV Unfractionated Heparin (UFH)5000 IU then 1250 IU/h should be started with confirmed diagnosis (absent pulse). Start before diagnostic procedures. Do NOT wait. Then chkAPTT (1.5-2.5 times abv pt’sbaseline)every 6hrs till 65-100 sec
+
Hx, PE = IV UFH = CT angio=>Surgery => DAPT/Antithrombotic
Surgical Mx:
*Emergency revascularisation -open thromboembolectomy, endarterectomy, bypass surgery, patch angioplasty, or intraoperative thrombolysis
*Paralysis/Paraesthesia: Definite Mx is Embolectomyunder 4hrs (after UFH)
After Surgery:
Patients who underwent angioplasty or stentingare typically placed on dual-antiplatelet therapywith aspirin (81 or 325 mg) + clopidogrel (75 mg)
Patients with underlying thromboembolic disease are typically anticoagulated with warfarin or a NOAC
WPW EKG =
SHORT QT SYNDROME causes
<350ms
HIPERCALCEMIA
CONGENITAL QT SYNDROME
DIGOXINA
HIPERKALEMIA ECG
SERUM k more than 9 mEq/l
TALL T WAVES
P FLAT WAVES
SHORT QT
(QRS LOOKS WIDE AND BIZARRE)
AMLODIPINO
AMIODORONA
complete heart block tx ?
first ATROPINE to stablize the patient once stable requieres the placement of a Pacemaker.
- atropina , transcutaneos pacing and transvenous pacing
- pacemaker
unstable=atropina
no cardioversion
no defibrilation
AV Blocks summary and treatment
Left bundel branch block
william
right bundle block
**marrow **
RSR’ v1-3
pulmonary embolism
extreme right axis deviation
S1 Q3 T3
(s en I pronunciada, q en 3 y t negativa )
cardiac arrest weeks later after miocardial infarction MOST COMMON ETIOLOGY =
VENTRICULAR FIBRILATION
Pericarditis
Anterior non STEMI
Right ventricular hypertrophy
left ventricular hypertrophy
Deep vein thrombosis
COST VMPF
virchow triad
WELLS SCORE
> =4 = DVT likely
diagnostic algorithm DVT
TREATMENT OF DVT
TREATMENT OF DVT
CONTRAINDICATION OF WARFARINE
DVT
Diagnostic algorithm for PULMONARY EMBOLISM
and PERC rule=?
Diagnosis PE
ekg
next step
imaging
Upper extremity DVT
SCV Syndrome
pericarditis etiology
Pericarditis
signs and symptoms
diagnosis of acute pericarditis
tretment of acute pericarditis
when hospitalization?
cardiac tamponade
becks triad
diagnostic and treatment cardiac tamponade
PREMATURE (ECTOPIC) VENTRICULAR COMPLEXES-
TX-
Pulmonary Embolism Clinical Features
Pleuritic Chest pain: Aggravated by cough and deep inspiration, worse with lying flat, relieved by sitting up.
Shortness Of Breath
Pulmonary Embolism
First Investigations (3)
Fist: Chest pain-ECG (S1Q3T3) Diagnostic
Second: SOB-CXR—> Rule out pulmonary pathology
Pregnancy (Doppler USD of legs)
Pulmonary Embolism
Best Investigations
Wells Score:
- Low: D dimer
- High: CTPA (Gold standard)
V/Q (Pregnancy or ♀< 45 yo)
Wells Score for PE (7 criteria)
Clinical symptoms of DVT (leg swelling, pain with palpation) 3
Another diagnosis less likely than pulmonary embolism 3
Heart rate >100 1.5
Immobilization (≥3 days) or surgery in the previous four weeks 1.5
Previous DVT/PE 1.5
Hemoptysis 1
Malignancy 1
Wells Score Probability for PE
Wells criteria
High >6.0
Moderate 2.0 to 6.0
Low <2.0
Modified Wells criteria
PE likely >4.0
PE unlikely ≤4.0
PERC rule (8 criteria)
- Aged <50 years
- Pulse <100 bpm
- SaO ≥95%
- No haemoptysis
- No oestrogen use
- No surgery or trauma requiring hospitalisation within 4 weeks
- No prior venous thromboembolism
- No unilateral leg swelling
RESULT: IF ALL YES RULE OUT PE
Pulmonary Embolism
Management
ABCD/Oxygen/Morphine
Stable:
- LMWH.
- Renal disease –> Unfractionated
Unstable: Thrombolysis
Acute Pulmonary Oedema (APO) Clinical Features
Sudden-onset of SOB with tachypnea
Diaphoresis and cyanosis
Productive cough: pink or white frothy sputum
Crackles and Wheezes (Kettle boiling)
- Hypotension: Cardiogenic shock
Acute Pulmonary Oedema (APO) Most common causes
- Acute Mitral and Aortic Regurgitation
- LV Systolic Dysfunction: anterolateral MI
- AF with rapid ventricular response
Acute Pulmonary Oedema (APO) Initial investigation
- CXR
- ECG
- Troponin
- FBE
- TTE
Acute Pulmonary Oedema (APO) Best investigation
Arterial/Venous Blood Gases to assess the severity of hypoxemia.
Acute Pulmonary Oedema (APO) Treatment
- O2
- IV line
- NGT spray or SL / IV is preferred to Morphine (BP > 100)
- Furosemide IV
- Morphine IV (chest pain)
- CPAP
APO + AF = BB
APO + AF + CHF = Digoxin inf
Order of most common microorganisms that cause infective endocarditis
- Staphiloccocus Aureus
- Streptococci
- Enterococci (at least 90% faecalis)
Infective Endocarditis RISK FACTORS
Artificial heart valves.
Congenital heart defects.
A history of endocarditis.
Damaged heart valves: rheumatic fever
History of intravenous (IV) illegal drug use.
Immunocompromised patient.
Infective Endocarditis Diagnose
Modify Duke’s criteria:
DEFINITIVE Infectious Endocarditis:
2 Major Criteria
OR
1 Major + 3 Minor Criteria
OR
5 Minor Criteria
POSSIBLE Infectious Endocarditis:
1 Major Criteria + 1 Minor criteria
3 Minor Criteria
In POSSIBLE Management: Repeat TTE + TOE
Modify Duke’s Major criteria
TWO MAJOR CRITERIA
- Positive blood cultures for infective endocarditis:
Typical microorganisms for infective endocarditis: Coxiella burnetii, Viridans streptococci, Streptococcus bovis, and HACEK group
OR
Community-acquired Staphylococcus aureus or enterococci in the absence of a primary focus.
NOTE: 2 blood cultures drawn 12 hours apart or all of 3 or most of 4 or more separate blood cultures, with the first and last drawn at least one hour apart
OR
- Evidence of endocardial involvement:
Positive echocardiogram for infective endocarditis
OR
Cardiac Vegetation
OR
Cardiac Abscess
OR
New partial dehiscence of prosthetic valve
OR
New valvular regurgitation
Modify Duke’s Minor criteria
FIVE MINOR CRITERIA
- Predisposing heart condition or intravenous drug user
- Fever: 38°C
- Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
- Immunologic phenomena:
Glomerulonephritis
Osler nodes
Roth spots
Rheumatoid factor (+) - Microbiologic evidence: positive blood culture but not meeting major criterion as noted previously or
echocardiography findings consistent with infective endocarditis but not meeting major criteria as noted previously
Infective Endocarditis Initial Investigations
- Blood culture: Diagnostic
- FBE: leucocytosis with neutrophilia and anemia.
- ECG: Cardiac monitoring
- CXR: Signs suggestive of heart failure.
NOTE: 2 blood cultures drawn 12 hours apart or all of 3 or most of 4 or more separate blood cultures, with the first and last drawn at least one hour apart
Infective Endocarditis Best Investigations
Transesophageal echo (TOE)
BUT:
- If HACEK: CT angio
- If arrhythmias: ECG
- If spread: CT/MRI (brain, thorax, and abdomen)
HACEK group
Slow-growing, fastidious gram-negative organisms
- Haemophilus species: Aggregatibacter aphrophilus, H. Paraphrophilus.
- Aggregatibacter actinomycetemcomitans
- Cardiobacterium hominins
- Eikenella corrodens
- Kingella kingae
COMPLICATED Infective Endocarditis include
Large vegetation
Perivalvular abscess
Multiple emboli
Secondary septic events
Infective Endocarditis Empirical Treatment
Benzylpenicillin + Gentamicin + Flucloxacillin IV
Infective Endocarditis Staphylococcus Aureus Treatment
Methicillin-susceptible:
Flucloxacillin x 6 weeks
Methicillin-resistant (MRSA):
Vancomycin IV x 6 weeks
ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks
Infective Endocarditis Streptococcus ADULTS Treatment
UNCOMPLICATED:
Benzylpenicillin + Genta IV x 2 weeks
OR
Benzylpenicillin IV x 4 weeks
OR
Ceftriaxone IV x 4 weeks
COMPLICATED:
Add gentamicin IV x 2 weeks
ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks
PROSTHETIC valve Streptococcus endocarditis Treatment
Benzylpenicillin x 6 weeks
Complicated: Add gentamicin IV
ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks
