Cardiovascular System
RATE AND RHYTHM DISTURBANCES SA Node Dysfunction
Sinus Bradycardia
Sinus Bradycardia
HR < 60/min with evenly spaced and normal width complexes.
Etiology
• Excessive vagal tone
• Hypothermia
• Hypothyroidism
• Depression of SA Treatment
Only when symptomatic or according to some also when HR < 40/minute. Atropine is first line of drug. Intravenous pacemaker is used if atropine fails to work.
(http://library.med.utah.edu/kw/ecg/mml/
ecg_brady.html) AV Block
First Degree AV Block
First Degree Block
PR interval on ECG > 0.20 sec at a HR of 70/min. Avoid β-blocker and CCBs.
Second Degree Block It is of two types:
Type I Block
• Type I/Mobitz type I/Wenckebach: Associated with digitalis toxicity, increased vagal tone and inferior wall MI. ECG features:
– PR interval increases until a P wave is completely blocked and a ventricular beat dropped.
– Next PR interval is shorter than the preceding one.
– RR interval goes on decreasing till the beat gets dropped.
– QRS complex is normal in width.
If it progresses to complete block, HR remains >
45/min with narrow QRS complex and Adams-Stoke*
attacks are uncommon.
Type II Block
• Type II/Mobitz II: Associated with anterior wall MI and also cases involving calcification of mitral or aortic valve annulus. There is no effect of carotid sinus pressure. ECG features:
– Suddenly a beat is dropped without any change in preceding PR interval, which remains normal in duration. If it is prolonged, the duration of prolongation remains fixed.
– RR interval of conducted beats usually remains constant.
Progression to complete block in this case leads to wide QRS complex and a HR < 45/min.
Adams-Stoke syndrome are commoner as compared to type I block.
Third Degree Block
Third degree/complete block: All atrial beats are blocked and ventricles beat according to an escape focus below the level of block.
Etiology
• Inferior or posterior wall MI.
• Ankolysing spondylitis with evidence of association with HLA-B27.
• Lenegre disease—It is fibrotic degenerative change in conduction system due to aging. It is commonest cause for complete block in adults.
• Inflammatory processes involving myocardium.
Clinical Manifestation
Adams-Stoke attacks-Circulatory arrest due to sudden asystole or ventricular tachyarrhythmias. Symptoms are assocoiated with these attacks or congestive failure occurs in patients with pre existing myocardial disease.
Treatment
First degree and type I second degree block may respond to IV atropine, which is normally used for reversing excessive vagal tones in emergency like acute MI. Complete heart block with slow ventricular rate can be given epinephrine or isoproterenol before setting up permanent pacing. Pacing is required in all symptomatic heart blocks.
‘99er’- Induction of mild hypothermia has been shown to improve outcome in comatose survivors of out-of-hospital cardiac arrest.
Supraventricular Arrhythmias
Sinus Tachycardia
HR > 100/min with normal width and evenly spaced complexes, but often P wave gets incorporated into preceding T wave. Transiently it is seen after discontinuation of β-blockers and usually due to conditions that increase heart rate like anxiety and fever.
Multifocal Atrial Tachycardia
PR interval and shape of P wave differs from wave to wave.
The rhythm is irregular with rates of 100-200 beats/min and there should be at least 3 different shapes of P waves for it to be diagnosed. It is seen in chronic pulmonary disease patients, old age people, hypokalemia, hypomagne-semia, valvular disease, aminophyllin.
Treatment: Therapy for multifocal atrial tachycardia is directed at treating underlying pulmonary disease and correcting electrolyte imbalances.
Paroxysmal Supraventricular Tachycardia
It (includes paroxysmal atrial tachycardia): Initiated by supraventricular premature beats, they are caused mostly due to re-entry through AV node. Often associated with perfectly normal heart. They are characterized by sudden onset and abrupt termination of tachyarrhythmias of regular rhythm with typically 160-220 beats/min which arise from ectopic sites.
Treatment: If carotid sinus massage done on only one side for 10-20 seconds in semi recumbent position fails, IV verapamil and adenosine are the drug of choice. Presence of carotid bruit is absolute contraindication for carotid massage. Other drug options are propranolol or IV digitalization. Radiofrequency catheter ablation is also a
very effective treatment option. Last resort is synchronized external cardioversion.
Atrial Flutter
Regular rhythm with a 2:1 block at AV nodal level leading to an atrial rate of 250-300 beats/min and a ventricular rate of 125-150 beats/min.
ECG: Saw-tooth pattern flutter waves most noticeable in the inferior leads.
Seen in alcoholics, thyrotoxicosis, mitral valve disease patients, COPD and pulmonary embolism patients.
Treatment
Digitalis or verapamil are the drugs used. In hemodynamically unstable patients synchronized cardioversion is used. The preferred treatment for recurrent atrial flutter is radiofrequency catheter ablation.
‘99er’- Synchronized cardioversion is done in atrial fibrillation, Supraventricular tachycardia and stable ventricular tachycardia.
Desynchronized cardioversion/defibrillation done in unstable/pulseless ventricular tachycardia and ventricular fibrillation.
Atrial Fibrillation (AF)
Atria beats at 350-500 beats/min and ventricle beats irregularly at slower rate. It is often seen as part of bradycardia-tachycardia syndrome. Commonly associated with thyrotoxicosis, rheumatic miral valve disease, CAD, cardiomyopathy, old age, alcoholics.
Atrial fibrillation is notorious for systemic embolization, which is very important entity to be taken care of during management of AF. Lone AF is one where no reason is found for it. In this case aspirin is enough to prevent stroke.
Treatment
Initial modality of choice is cardioversion.
Pharmacological treatment includes IV digitalis, propranolol, IV verapamil. If still persists, quinidine and procainamide may be used. Procainamide and ibutilide are the drugs of choice in the treatment of preexcited atrial fibrillation. Ask the patient to stop alcohol.
To prevent embolism, warfarin therapy should be started 3 weeks before cardioversion and should be continued for atleast 4 weeks after normal rhythm is achieved. But in low-risk patients with lone atrial fibrillation, warfarin anticoagulation is not required.
Aspirin or no therapy is recommended in these patients.
Sometimes, a heparin therapy bridge is required after stoppage of warfarin therapy and before a major surgery.
High risk patients that require a heparin anticoagulation bridge include those with a mitral mechanical valve, atrial fibrillation, or previous embolism.
‘99er’- In patients on warfarin who develop a microcytic anemia, a gastrointestinal lesion should be suspected.
‘99er’- Atrial arrhythmias are a common indication of repaired tetralogy of Fallot residua. Long-term regular follow-up is required in all patients with repair of complex congenital heart disease.Pulmonary valve regurgitation is the most common long-term complication following surgical treatment for tetralogy of Fallot
Ventricular Arrhythmias
Premature ventricular contractions: Common in healthy adults and is not a cause for concern. Their suppression is indicated only in patients with severe and disabling symptoms.
When 3 or more consecutive beats of ventricular origin are at rate > 120 beats/min. AV dissociation is present. They
are mostly of re-entrant type. VT is common in CAD, cardiomyopathies, MVP, metabolic derangements, digitalis toxicity, hypothermia. Long QT syndrome may also cause VT. It is commonly seen after acute MI. VT that persists for more than 30 seconds is called sustained VT.
Clinical Features AV dissociation leads to:
• Canon waves-intermittent peaks in jugular venous pressure when atria and ventricle beat together.
• Variation in intensity of heart sound, along with some extra heart sounds.
• Variations in systolic BP.
Other associated features are that of CHF, light headedness, hypotension, syncope. Widely split S1 S2 is heard because of asynchronous excitation of two ventricles.
ECG Features
No P waves are visible. QRS complexes are bizarre in shape and wide.
Treatment
VT patient with no pulse is treated on lines of ventricular fibrillation.
Stable VT—Amiodarone or lidocaine are the first drug of choice for rate control. Procainamide can be given if they fail. Use cardioversion if patient becomes unstable anytime.
Unstable VT: Cardioversion is done. Start with 100 J and subsequently use 200 J, 300 J and 360 J.
For idiopathic ventricular tachycardia with refractory symptoms, radiofrequency catheter ablation has an excellent cure rate.
Torsade De Pointes
It is a form of VT in which ECG varies with an undulating amplitude, which makes it seems like an ECG twisting around a point. It may progress on to ventricular fibrillation.
Etiology
• Hypokalemia and hypomagnesemia
• Subarachnoid or intracerebral hemorrhage
• MI or myocardial inflammation
• MVP
• Drugs that prolong ventricular repolarization like disopyramide, procainamide, quinidine, pheno-thiazines, TCA, lithium, thioridazine.
Clinical Features
Patients are prone to dizziness and syncope. Sudden auditory stimulation like even phone ring at night may precipitate torsades in vulnerable patients with long QT interval syndrome.
Treatment
Cardiac pacing or IV isoproterenol is used for emergency treatment. Do cardioversion in hemodynamically unstable patients. In stable non emergent cases correct the underlying disorder or use antiarrythmic drugs that do not affect or prolong ventricular repolarization like lidocaine or phenytoin.
‘99er’- TCA- inhibits fast Na+ channels and prolongs QRS and re-entrant arrhythmia. Most effective treatment is sodium bicarbonate. Lidocaine is drug of choice in TCA induced ventricular dysarythmia.
Ventricular Fibrillation (VF)
Electrical activity on ECG but no organized pattern.
Etiology is almost same as VT.
Clinical Features
An unresponsive patient with VF on ECG.
Treatment
After primary ABC survey, do CPR until defibrillator is ready. Defibrillate with 3 shocks of 200 J, 200-300 J and 360 J. Then again check for rhythm after shocks. If VF persists, do detailed secondary survey and give Epinepherine (1 mg IV every 3-5 mins) or vasopressin (40 U IV, single dose). If still no response, again defibrillate with a 360 J shock. After this consider antiarrythmics like lidocaine, amiodaone, procainamide or magnesium (if hypomagnesemia). Intravenous amiodarone is the drug of choice for shock-resistant ventricular fibrillation. If still no success, continue to defibrillate.
Wolff-Parkinson-White (WPW) Syndrome It is a pre-excitation syndrome in which a portion of ventricle is excited by an atrial impulse earlier than the impulse through normal conduction pathway. It is associated with congenital cardiac defects like Ebsteins anomaly or transposition of great vessels, PSVT, AF and atrial flutter, cardiomyopathy.
ECG: Wide QRS with characteristic delta wave which is due to pre-excitation. It also shows short PR interval (< 0.12 second), which is a manifest of pre-excitation. If β-blocker or verapamil are given to the patient, it may change into VF.
‘99er’- Short PR interval is associated with loud S1.
Treatment
Procainamide is used if patient is hemodynamically stable.
In unstable patients, immediate synchronized cardioversion is used.
CCBs and digoxin should be avoided in these patients, as they inhibit conduction in normal conduction pathway and that may cause VT or supra ventricular arrhythmias.
‘99er’- Adenosine is the treatment of choice for narrow-complex tachycardia. Procainamide is the drug of choice for wide-complex tachycardia of unclear etiology. Neither adenosine nor other AV nodal blocking agents should be given to patients with pre-excited tachycardias.
‘99er’-Biventricular pacing improves cardiac performance and quality of life and may also improve
survival. An implantable cardioverter-defibrillator (ICD) is indicated for patients with left ventricular dysfunction and hemodynamically significant ventricular arrhythmias.
‘99er’-Metastatic cardiac malignancy: The epicardium is the most common location of metastatic cardiac neoplasm. Breast and lung carcinoma are the most common causes of malignant pericardial disease.
‘99er’-Although uncommon, left atrial myxoma should be considered in young patients with embolic stroke. It is most common cardiac tumor. More common in women and involves lest atrium in 80% of cases. May present with systemic illness mimicking infective endocarditis or with signs and symptoms of mitral valve obstruction. Sometimes it produces a diastolic sound due to tumor motion (tumor plop).Echocardiography is an important imaging modality for diagnosis of such an intracardiac tumor.
Pregnancy and Cardiovascular System Dysfunction
Functional status before pregnancy is a strong predictor of maternal risk. A systolic murmur, an S3 gallop, and mild peripheral edema are normal findings during pregnancy.
• Spontaneous coronary artery dissection may occur during pregnancy.
• Valvular disease: An additional hemodynamic stress during pregnancy (e.g. tachycardia) may precipitate symptoms in women with severe valve obstruction.
Regurgitant valve lesions are well tolerated in pregnancy. Continuous effective anticoagulation is needed throughout pregnancy in women with mechanical heart valves.
• Women with Marfan syndrome are at increased risk of aortic dissection during pregnancy and it should be considered in the differential diagnosis of chest pain in pregnancy.
• The use of angiotensin-converting enzyme inhibitors should be avoided during pregnancy.
• Hydralazine and nitrates are the vasodilators of choice to treat heart failure during pregnancy.
• Eisenmenger syndrome places women at an extremely high maternal risk.
‘99er’-α-hydralazine/nitrate combination should be considered in patients with heart failure who develop hyperkalemia while taking an ACE inhibitor or an ARB.
‘99er’- Statins- should be stopped if CPK level > 10 times the normal level. The chances of statin induced myopathy increases if they are taken along with fibric acid derivatives.
‘99er’- Atrial tachycardia with variable block is a classic electrocardiographic finding in digitalis toxicity.
The first-line treatment for life-threatening digitalis toxicity is administration of digoxin-specific antibody fragments.
‘99er’- Amiadarone’s most feared and life threatening side effect is pulmonary fibrosis. Other side effects are skin discoloration and hypotension (with IV formulation). It also increases warfarin life and warfarin dose needs to be decreased.
Bile acid binding resin-cholestyramine
When Systolic BP < 90 mm of Hg
In patients who had a cardiac index below periodic LFT and look out for ↑ CPK levels (muscle damage)
Aspirin before dose ↓ flushing
Most patient are not able to tolerate GI effects
Viagra (shouldn’t be used within 24 hours of nitrates or vice versa) Metoprolol, atenolol, propanolol(all three also in angina) and timolol approved for long term use after MI
May be harmful to post MI patients if patient already has LV failure.
Heparin induced when given along with statins effect on lipid profile Ticlodipine causes
↓ LDL (first line agents)
↓ triglycerides, slightly ↑ HDL follow up therapy to tPA
Contd...
Drugs Thrombolytics(tPA, streptokinase, reteplase)
ACE inhibitors
Cardiac glycosides-digoxin
Thiazides (distal tubular action)
Indication Within 12 hours of MI pain, new left bundle branch block
Post MI patients, CHF
CHF, paroxysmal atrial tachycardia (PAT), AF
CHF, edema
Adverse effects Bleeding, reperfusion arrhythmias
Cough, angioedema, taste change, rash, hypotension, hyperkalemia Digitalis toxicity-nausea, vomiting, blurred vision, yellow vision, arrhythmias (particularly PAT), gynecomastia.
TREATMENT-stop drug, give K+, lidocaine, phenytoin, digitalis antibody (in acute overdose)
Metabolic alkalosis, hyponatremia, hypokalemia, hypercalcemia, thrombocytopenia, ↓ K+, ↑ CA++,
Contraindication Dissecting aortic aneurysm, recent stroke, recent surgery
Pregnancy, bilateral renal artery stenosis
Misc. fact They do not cause anti coagulant state.
Streptokinase may cause anaphylaxis if previously exposed.
First line drug in CHF.
Decrease mortality.
Predisposers to toxicity:
↓K+, ↑ CA++, ↓ Mg++, renal insufficiency, SA and AV block,
hypothyroidism, old age, WPW.
Contd...
# ‘99er’-β-blockade does not promote clinical claudication.
* ‘99er’-β-blockers should not be initiated in heart failure patients who are acutely decompensated or volume overloaded.
FLUID AND ELECTROLYTE DISORDERS