Remember

In constrictive pericarditis and tamponade, catheterisation shows the same diastolic pressure in all 4 chambers!

TOF

Tetralogy of Fallot
Pulmonary stenosis+ VSD+overriding aorta+RVH

Cyanotic congenital heart disease (The 5 Ts. others are TGA, Truncus arteriosus, Total anomalous pulm venous return, Tricuspid atresia)

Right to left shunt leads to mixing

May not be cyanotic at birth

Difficulty feeding, polycythaemia, finger clubbing, dyspnoea, FTT, murmur

Tet spells
sudden, marked increase in cyanosis followed by syncope ,often precipitated by crying, feeding or exercise , may also occur on waking up.
It is due to an increase in rt to left shunting of unoxygenated blood following a decrease in systemic vascular resistance or increased pulmonary vascular resistance, favouring the "right to left to aorta shunt"
It can be relieved by squatting or placing child in knee chest position (This increases afterload thus allowing more blood to go thru pulmonary circulation rather than systemic)


Chest x ray shows boot shaped heart and decreased pulmonary vascular markings.

Treatment of Primary pulmonary hypertension

Mgt:
IV vasodilator  challenge (prostacyclin, NO, adenosine) in order to decide definitive treatment

Definitive treatment:
If responsive to vasodilator challenge, start Calcium channel blockers. Try for at least 3-6months, if no response use prostacyclin

If no response to vasodilator challenge, other modalities including Transplant depending on the NYHA classification

Anticoagulation for all patients (Warfarin)

Remember

Patient with sudden onset cardiac decompensation with acute pulmonary edema should have an ECG done first before any medications, to rule out arrhythmia e.g atrial fibrillation which may require immediate synchronised cardioversion.

If no arrhythmia, then reduce preload with diuretics, nitrates and morphine.

Remember

For all left heart stenotic murmurs, reducing preload (e.g diuretics) prolongs devt of pulmonary congestion

For all left heart regurgitant murmurs, drug treatment is aimed at reducing afterload (vasodilators)

For mitral valve prolapse, drug treatment (if symptomatic), is aimed at increasing preload (propanolol)

For hypertrophic cardiomyopathy, increasing preload reduces the murmur( squatting increases VR, beta blockers and calcium channel blockers allow more ventricular filling)

note: Valsava manoeuvre increases afterload, reduces preload. It therefore increases intensity of murmur in aortic stenosis but reduces the intensity in HCM.

Remember

Fixed splitting of S2 = ASD

Coronary artery bypass graft

Indicated in patients with CAD with angiography showing >70% stenosis of left main coronary artery or >70% stenosis of 3 or more vessels (2 or more vessels if diabetic)

Internal mammary artery graft preferred over saphenous vein graft (restenoses in abt 5 yrs)

Complications post MI

Sinus bradycardia : give atropine if symptomatic

3rd degree AV block:  Usually ffing Inf wall MI (ST elevation in leads II, III and avf) - bradycardia, there's independent contraction of RA and RV leading to Canon A waves (in Jugular). Treatment is pacemaker

Right Ventricle infarction: (also Inf Wall MI), RV dysfxn leads to reduced pulmonary bld flow, low preload, hypotension especially with nitrate use, tachycardia. Lungs are clear.Tmt is high volume fluid infusion. Avoid nitroglycerin
(vasodilator).

Ventricular fibrillation/tachycardia: loss of pulse, ECG findings. Tmt: defibrillation if no pulse

Reinfarction: recurrence of pain, new signs of pulmonary edema, new rise in CK-MB (Troponin is useless high cos level remains high for 10-14 days after initial infarction unlike CK-MB- 1-2 days) Tmt: As new MI

Free wall rupture: usually 2-8 days post MI when scars are forming but can occur as early as within the first 24hours, leads to cardiac tamponade, hypotension, JV distension, sudden loss of pulse. Do Echo. Tmt: emergency pericardiocentesis then surgical repair

Septal rupture: septal defect forms, new pansystolic (VSD) murmur hrd best at LLSB, pulmonary congestion, step up in oxygen saturation as you move from right atrium to right ventricle. Do Echo

Valve rupture: valvular insufficiency, mitral regurgitation, new systolic murmur heard best at apex radiating to axilla. Do Echo


edited: mechanical complications (rupture) can occur as early as the first day of MI although more common days and weeks after.

Treatment of heart block

First degree (prolonged PR) :
No treatment


Mobitz I (prolonged PR, longer PR, even longer PR then dropped beat, cycle repeats. could be 2:1,3:1, etc.):
Treat underlying cause


Mobitz II (Just dropped beats. Constant PR intervals,no prolongation of PR with subsequent beats as in in type I):
Pacemaker


3rd degree (No relationship between P and QRS waves and the P rate is faster than QRS rate):
Pacemaker

Atropine is used in first degree and Mobitz I if the bradycardia is severe or symptomatic.
IV Atropine is first line in any severe symptomatic bradycardia.

Treatment of stable angina

i.e angina precipitated by exertion, relieved by rest

Stable angina is as stable and simple as A, B, Cerine!

A- aspirin
B- beta blocker
C- nitroglycerine

Treatment of ST segment depression / Unstable angina

Aspirin (or clopidrogel or prasugrel): prevents plaque rupture

Heparin: prevents further growth of thrombus

then

Nitroglycerin
Morphine
Oxygen
Beta blockers
ACEi
GP2a/3b inhibitors


No mortality benefit from Oxygen, Morphine or Nitrates
No need for thrombolytics in non ST seg elevation event. Just prevent further elongation by giving heparin.

Treatment of STE Myocardial infarction (STEMI)

Aspirin (or if allergic, clopidrogel or prasugrel)

next

Angioplasty (door to balloon time 90mins) or if not available, thrombolytics (door to needle time: 30mins)

• Angioplasty (PCI) is preferable to thrombolytics however in the absence of PCI, give thrombolytics preferably within 30mins of infarction, but can still be given up to  12hrs post MI

then

Beta blockers (if contraindicated then use CCBs)
ACEi/ARB (especially with ejection fraction <40%)
Oxygen
Statins (especially with LDL >100mg/dl)



WARFARIN IS USELESS IN MI TREATMENT
Heparin can be administered for a short time post angioplasty to prevent restenosing 

Treatment of Pulmonary embolism

1. Anticoagulation: Heparin + Warfarin. Stop Heparin after 5-7 days when Warfarin may've kicked in. Target is INR of 2-3

2. IVC filter:
if heparin is contraindicated
if recurrent embolic event even while on heparin or therapeutic Warfarin (INR 2-3)
if there's severe disease with right ventricular dysfxn and enlargement. The next embolus could be fatal so put a filter


3. Thrombolytics (t-PA- tissue plasminogen activator): if patient is too unstable or if there's RV dysfxn

Aspirin is useless in PE

Note: watch out for HITT with heparin therapy. - monitor cbc
HITT:
Patient on heparin
Thrombocytopenia
5-10 days after start of treatment
New thrombus or expansion of old one
Mgt: stop heparin, give thrombin inhibitor: Argatroban or lepirudin

Do not transfuse platelets in HITT

Remember

Check TSH and T4 in every patient with new atrial fibrillation  
 (? HYPERTHYROIDISM)

Check TSH and T4 in every patient with hyperprolactinemia    
(? HYPOTHYROIDISM)

Check TSH and T4 in elderly patient with sudden dementia + new hypercholesterolaemia +decreased deep tendon reflexes , constipation, weight gain etc
(? HYPOTHYROIDISM)

Superior vena cava syndrome

Suspect in patient with history and findings suggestive of bronchogenic carcinoma, with

shortness of breath
face or arm swelling
headache
upper chest vein distension
neck vein distension


Due to compression of SVC by tumour

Ventricular tachycardia

Life threatening!

Tachcardia + wide QRS (diff from a specific SVT called wide QRS SVT, however better to consider and treat as VT until proven otherwise)

Causes include electrolyte abnormalities, MI, drugs, long QT syndrome etc

Tmt: Immediate cardioversion-

If stable: Chemical (Amiodarone , Lidocaine) or Sync DC cardioversion

If unstable: has pulse- Synchronised DC cardioversion
                   no pulse - defibrillation


Note:
 Torsades de pointes :

is a different type of VT. The morphology of QRS varies from one complex to the other thus it's refered to as polymorphic VT. 
Caused by anything that can prolong QT interval. culprits include Quinidine, Procainamide, Sotalol, Amiodarone (least likely) etc

Tmt includes Magnesium sulphate infusion first!

Paroxysmal supraventricular tachycardia

Sudden onset palpitation
Dizziness
Chest pain
Dyspnea
+/- LOC

Due to

• AV node re-entry or
• AV  re-entry  (av node + accessory pathway)- WPW syndrome

ECG : Tachycardia + narrow QRS, retrograde P wave -right after QRS


In WPW, there's the Delta wave- slurred upstroke of the QRS with a short PR interval bcos the signal evades the normal AV node delay and rather passes thru the accessory pathway.

Treatment:
Initial: vagal maneouvres (vasalva, carotid massage)

Drug Tmt :
Adenosine to block AV node except for Wolff-Parkinson-White (AV blockers  r contraindicated in WPW becos it'll only promote passage thru accessory pathway.) Amiodarone for WPW

2nd line drugs include verapamil, diltiazem, metoprolol, digoxin

Cardioversion for unstable patients or those not responsive to medications.

Aortic Dissection

Severe, tearing chest pain, radiating to the back/inter-scapular area
Hypertension (or hypotension)
Asymmetrical BP
BP lower in rt arm if tear extends into brachiocephalic artery
BP lower in left arm if tear extends into left Subclavian
signs of ischemic stroke if tear extends into common carotid
New murmur if aortic regurgitation, due to aortic root involvement

Best initial test is CX-ray : widened mediastinum
TEE more sensitive
Most accurate test however is angiography (but is not usually necessary and carries higher risks)

Tmt of Ascending aortic dissection is emergent surgery
Tmt of Descending aortic dissection is BP control first! Beta blocker to reduce shearing force then Nitroprusside.
Don't give Nitroprusside before Beta blocker in aortic dissection.