Flashcards in Cardiology Deck (53)
What are the different types of heart block?
PR interval of >0.12s
Mobitz I block:
Increasing PR interval until p waves fail to conduct
Mobitz II block:
dropped QRS not preceded by a p wave, normally in a 2:1 or 3:1 pattern. Every 2nd or 3rd p wave conducts to the ventricles.
Complete heart block. The atrium is not conducting to the ventricles at all. Rate normally very slow (~30 bpm) Can cause syncopal attacks.
What are stokes- adams attacks?
Syncopal attacks caused by a transient rapid tachycardias arising at the onset of complete heart block.
What are the indications for temporary pacing?
Symptomatic bradycardia that is unresponsive to atropine
After an anterior MI if the patient is in type 2 or 3 heart block
To suppress drug resistant tacharrhythmias
What are the indications for a permanent pacemaker?
Complete heart block
Mobitz type II block
persistent AV block post MI
drug resistant taychcardias
What do the three letter codes mean with regards to pacemakers?
1st letter = chamber paced, Atria, Ventricle of both (D)
2nd letter = chamber sensed, A, V, D or none (0)
3rd letter = pacemaker response, Triggered, Inhibited, Dual, Reverse
What are the complications of a pacemaker insertion?
Pneumothroax, wound haemotoma or dehiscence
Describe the wave form of the JVP
3 peaks (a, c and v) and 2 troughs (x and y descents)
a wave = produced in atrial systole
increased with RV hypertrophy. giant canon waves occur in complete heart block and VTs
x descent = when atrial contraction finishes. Ventricular systole.
c wave = occurs during x descent and is due to the right ventricular systolic pressure transmitted before the tri-cuspid valve closes.
v wave = venous return filling the right atrium. giant v waves occur in TR
y descent = when the tricuspid valve opens.
A steep y descent occurs when there is tricuspid incompetence or constrictive pericarditis
What are the characteristic ECG changes in pericarditis?
Saddle shaped ST elevation - there is a concave upwards
in 10% the ECG is non specific or normal
Name the causes of acute pericarditis:
Viruses - coxsackie, flu, epstein barr, mumps, varicella, HIV
Bacteria - pneumonia, rheumatic fever, TB, staphs, strep
Post MI - Dressler's (2- 10 weeks post MI the body creates auto-antibodies and pts get recurrent pericarditis)
Drugs - procainamide, hydralazine, penicillin, isoniazid
Others - ureamia, RA, SLE, myxodema, trauma, surgery, malignancy, radiotherapy, sarcoidosis
What are the clinical features of pericardial effusion?
Dyspnoea, raised JVP, bronchial breathing in left base - Ewart's sign = large effusion compressing the left lower lobe
What is cardiac tamponade?
Accumulation of pericardial fluid that raises the intra-pericardial pressure and results in poor ventricular filling and a decrease in cardiac output
What are the signs of cardiac tamponade?
Increased pulse, low BP, pulsus paradoxus - increase in pulse on inspiration, Kussmaul's sign - JVP rise with inspiration, muffled S1 and S2.
Beck's triad = falling BP, rising JVP, small quite heart
What causes constrictive pericarditis?
a rigid pericardium - interferes with diastolic filling so causes signs of R heart failure:
increased JVP, systemic venous congestion, pulmonary congestion, Kussmaul's sign, soft diffuse apex beat, quiet heart sounds, S3,
MUST distinguish from constrictive cardiomyopathy
What is a 3rd heart sound and what does it signify?
Heart sound in diastole, making a galloping rhythm.
Occurs as a result of rapid relaxation of the ventricles and occurs in heart failure
What are the causes of acute myocarditis?
Viral - flu, hepatitis, mumps, rubella, Coxsackie, poli, HIV
Bacterial - Clostridia, diptheria, TB, meningococcus,
Spirochaetes - leptospirosis, syphilis, lyme
Protazoa - Chagas'
Drugs - cyclophospamide, herceptin, penicillin, chloramphenicol, methlydopa, spironolactone,
What is hypertension?
A sustained BP of >140/90
Who gets treated for hypertension?
BP > 160/100
BP 140/90 with CHD and stroke risk or target organ damage
What is malignant hypertension?
BP >200/130 + bilateral retinal haemorrhages (papilloedmea doesnt have to be present)
What are the causes of hypertension?
Essential - no known cause
Renal disease - intrinsic renal disease or renovascular disease (atheromatous or fibromuscular dysplasia)
Endocrine - cushings, Conns, phaeochromocytoma, acromegaly, hyperparathyroidism
Others - coarctation, prenancy, steriods MAOIs, the pill
What is the end organ damage from HTN?
LVH, retinopathy, kidney disease
What is the target BP for patients with diabetes?
<125/75 if proteinuria
Which antihypertensives do you use?
Pt 55yrs or black origin of any age:
Ca Channel blocker, followed by ACEi, followed by thiazide duiretic, then consider increasing the duiretic, adding spironalactone or a B blocker
What are the two types of infarction that usually occur in a MI?
Transmural - full or near full thickness infarction of the ventricular wall usually in the distribution of an coronary artery.
Associated with atherosclerosis, plaque rupture and super imposed thrombosis
Subendocardial - 1/3 - 1/2 of the venticular wall
Due to diffuse stenosisng arthersclerosis and global reduction in coronary flow ie due to shock
Describe the histopathological changes that occur between initial event and 8 weeks after an MI
20-40mins - ultrastructural changes of irreversible damage
2-3hrs - staining with tetrazolium dyes
4-12hrs - classic necrosis
12-24hrs - gross alterations with the naked eye
2-3 days - acute inflammation
5-10 days - macrophages remove necrotic muscle cells
2-4 weeks - granulation tissue most prominent
6 weeks scaring well advanced
>8 weeks cannot tell whether the event was 8 weeks ago or 10 yrs.
When do the different cardiac enzymes rise after an ACS?
Trop - rises within 3-12hrs with a peak at 24-48hrs, falls back to baseline over 5-14 days
CK -MB (cardiac specific) - rises withing 3-12hrs, peaks at 24hrs and falls again after 48-72hrs
Myoglobin - rises within 1-4 hrs of the pain
very sensitive but not specific
LDH rises at day 2 and peals at day 3
What are the complications of an MI?
Bradycardia/ heart block:
1st degree most commonly after inf MI
complete AV block usually resolved after a few days
keep K an Oxygen levels within normal range
from LV mural thrombus
1. severe LV dysfunction causing annular dilation of valve
2.MI in inf wall leading to papillary muscle dysfunction
3. MI in papillary muscles
Ventricular septal defect:
Pansystolic murmur, high JVP, cardiac failure
caused by rupture of the myocardium due to remodeling of the tissue.
Left ventricular aneurysms
recurrent pericarditis, pleural effusions, fever and anaemia
What are the causes of atrial fibrillation?
Heart failure/ ischemia
Mitral valve disease
Low potassium, low magnesium
sick sinus syndrome
LONE AF = no cause found
What are the two types of cardioversion?
Electrical cardioversion = using defib
Drug cardioversion = amioderone IVI 5mg/kg over 1hr via central line or flecanide if there is no structural cardiac disease, or WPW (it is a strong negative inoptrope)
Do not cardiovert until fully anticoagulated if the AF has been going on for >48hrs
What is the difference between rate control and rhythm control in atrial fibrillation?
usually used first line in patients with AF unless the AF had a reversible cause, a patients heart failure is thought to be primarily caused by their AF, it is new onset AF, the AF is thought to be suitable for ablation
B blocker is first line or a rate limiting Ca blocker, can add digoxin or diltiazem if doesn't respond.
Aim is to get HR <100 so they can carry out physical activity.
If cardioversion is chosen should anticoagulate and use amioderone for 4 week beforehand, and continue up to 12 weeks.