Cardiac Flashcards
Prinzmetal angina
“Variant” or “vasoapastic angina”
AICD
Automatic implantable cardioverter/ defibrillator
Inferior wall MI
12 lead: II, III, and aVF
-reciprocal: I, AVL
-affects the RCA (supplies blood to the AV node) = conduction deficits and heart blocks
Anterior wall MI
12 lead: V2-V4 (anterior) -reciprocal: II, III, AVF V1 & V2 (septal) May see BBB, and AV block type II -reciprocal: V5-V6
-affects the LAD (left main/ widow maker)
Lateral wall MI
12 lead: I, aVL, V5& V6
Reciprocal: II, III, AVF
-affects the left circumflex and the obtuse marginal artery (a branch of the circumflex)
Posterior wall MI
12 lead: V7-V9 (right sided 12 lead)
Reciprocal: V1-V3
-affects RCA
CARDIAC INDEX
2.5-4.5 L/min
CARDIAC OUTPUT
5-6 L/min
*stroke volume x HR
PRELOAD
“Filling”
-pressure generated by the volume of blood at the end of diastole
*RV:
CVP (N: 0-5 mmHg, optimal 0-10)
RAP
*LV: (by arterial pressure monitors)
-PAD, LVEDP
-affected by venous return, total blood volume, atrial kick, and ventricle compliance
AFTERLOAD
“Resistance”
-pressure and stress the ventricle faces
- RV: PVR (pulmonary vascular resistance)
- more sensitive
*LV: SVR (systemic vascular resistance)
- *⬆️afterload = ⬆️ myocardial O2 demand
- *⬇️afterload by ⬇️SVR (vasodilator, ⬇️ blood volume, repair leaky valve)
RAP
Right atrial pressure
2-6mmHg
*measures pressure in the right atrium by a PA cath
Elevated in RV failure
*reflective of RV preload
CVP
Central venous pressure, catheter in superior vena cava
*measures pressure in the great vessels as blood returns to the heart
Normal: 0-5mmHg
Optimal: varies- 10 mmHg
-depends on MD
Tells about preload in the RV
PAOP
Pulmonary arterial occlusion pressure (wedge pressure)
Normal: 6-12 mmHg
Optimal: 14-18 mmHg
Tells about preload in the LV
SVR
Systemic vascular resistance
Normal: 800-1200 dynes/sec/cm
SVRI: 1970-3900
Measures afterload
PVR
Pulmonary vascular resistance
Normal: <250 dynes/sec/cm
Pulmonary artery pressure
Normal:
Sys:15-25/
Dia: 6-12
PAs: reflective of RV (pressure needed to open the pulmonic valve)
PAd: reflective of the pulmonary vasculature
Difference between PAD and PAOP
“Right to left gradient”
PAD > PAOP by 5 mmHg or less
If difference>5 =pulmonary HTN
CARDIAC Tamponade
- equalization of pressures (RAP, PAD, PAOP)
- large A waves and V waves=M pattern on waveform
- hypotension
Pulmonary hypertension
⬆️PAD, and PAOP= normal
Mitral regurg
- large V waves in PAOP waveform
* due to acute MI
Classes of antidysrhythmics
I: block the movement of sodium during depolarization
-ex: quinidine, procainamide, lidocaine
II: block beta receptors (affect automaticity)
-ex: metoprolol, propranolol
III: block the movement of potassium (during late depolarization)
-ex: amiodarone
IV: blocks movement of Ca (during early depolarization)
-ex: diltiazem, verapamil
Nesiritide (Natrecor)
Vasodilation
Is a brain-type naturiuretic peptide (BNP)
Causes excretion of sodium and water
(Diuretic effect)
First line therapy for HTN
Diuretics
Then BB
Then ACE inhibitor
Stenosis & Regurgitation
REMEMBER BLOOD DOES NOT TRAVEL UPHILL
ABI
Ankle Brachial INDEX
Ankle artery pressure (normally is higher) divided by brachial artery pressure
Normal= >1
*ankle artery pressure decreases long before pulses are lost
Dilated cardiomyopathy
S& S:
- mitral regurg (dt vent dilation and stretching of mitral valve ring)
- hypotension
Restrictive cardiomyopathy
S& S:
-elevated sedimentation rate (dt inflammatory response from connective tissue disorders)
Hypertrophic cardiomyopathy
Heart muscle enlarges causing ventricle walls to thicken
- can cause regurg
- associated with obstruction and poor outflow
S& S: syncope
Treatment: decrease contractility and afterload
S3
Ventricular gallop
“ken-tuc-KY”
Cause: left ventricular failure (earliest finding)
Indicates HF and fluid overload
Occurs at the beginning of diastole
S4
Occurs during the end of diastole
-when the atria contract but the ventricle is noncompliant
Atrial gallop
“TEN-nes-see”
Cause:
-myocardial ischemia, infarction, severe hypertension, and hyper trophy
*normally heard in acute MI for the first 48 hours
Atrial enlargement
*leads II, and V1 are the best P wave leads
R atrial enlargement: P waves tall and peaked in lead II (P PULMONALE), dominate initial half of biphasic P in V1
L atrial enlargement: P waves wide and notched (P MITRALE), dominant terminal half of biphasic P
Automaticity
Ability of certain CARDIAC cells to initiate impulses regularly and spontaneously
Enhanced automaticity: causes ectopic beats and is associated with catecholamines
Triggered activity
Related to depolarization problems
Causes torsades de pointes
Accessory pathways
Causes palpitations, tachydysrhythmias
Reentry
Most common mechanism for tachydysrhythmias
Propranolol
Non cardio selective BB
Not to be used in PTs with COPD or asthma (causes further bronchospasms
Cardioselevctive BB: metoprolol, atenolol, and esmolol
Diacritic notch
Arterial waveform= closure of the aortic valve
Pulmonary artery waveform= closure of the pulmonic valve
Transient systolic murmur
Papillary muscle ischemia and dysfunction
Midsystolic click
Mitral valve prolapse
Paradoxical split of S2
L BBB, RV premature ventricular contraction, transvenous endocardial pacemaker, valvular problem
Split S2
Normal: only split on inspiration
Abnormal: split in expiration
More common than a split S1
Supra ventricular tachycardia with aberrancy
A run of wide QRS complexes triggered by a PAC
vTach= a run of wide QRS complexes triggered by a PVC
R BBB
Wide QRS (>.12)
V1: QRS has rsR “M” or bunny ear pattern
V6: slurred S wave
L BBB
QRS wide (>.12)
V1: QRS is negative
V6: QRS is rsR
Barorecptors
PRESSURE RECEPTORS!!
Vasodilators= stimulation of barorecetors
-can cause reflex tachycardia
