CCRN- Cardiac Flashcards
(43 cards)
Indications of successful reperfusion following PCI or IV thrombolytic therapy?
- pain cessation
(blood flow ends the anaerobic metabolism and production of lactic acid) - increase in CK or troponin
(the rtn of blood flow can result in a “reperfusion injury” of muscle raising biomarkers; CK “washout”) - reversal of STE w/ return to baseline
- short runs of VT (caused by O2 free radicals, myocardial stunning when vessel opens)
Why is propranolol not given, but metoprolol is for a patient c/o CP, having an MI?
Beta blockers help decrease the workload of the heart and increase the threshold for Vfib, however propranolol is not cardio selective. Propranolol affects Beta 1 heart and Beta 2 lungs so it s more likley to cause bronchoconstriction than a cardio selective BB.
Metoprolol is cardioselective and the drug of choice.
-> Contraindications: bradycardia, hypotension, and use of phosphodiesterase-inhibitor drugs
Eligibility for tx of STEMI?
- STE in 2 or more contiguous leads or new onset of LBBB
- Onset of CP <12hrs
- CP of 30min in duration
- CP unresponsive to SL NTG
**If onset < 12hrs = REPERFUSION
PCI; door to balloon = 90min
Fibrinolytic: Door to drug = 30 min
If patient vasovagals with sheath removal, what are the interventions?
fluids and atropine
- -SBP <90 w/ or wo bradycardia, absence of compensatory tachycardia
- -pallor, nausea, yawning, diaphoresis
Signs of retroperitoneal bleeding
sudden hypotension
severe low back pain
Need to give fluids & blood products (patient bleeding!)
Inferior MI
II, III, aVF
(reciprocal in lateral I, avL) - ST depression;
reciprocal in V1-V2 indicates posterior MI as well«<
RCA occlusion (also supplies RV)
**Associated w/ AV conduction disturbances:
-2nd Type I AVB
-3rd degree AVB (need pacemaker)
»>REMEMBER: INFERIOR 3, 2, 1 for 3rd degree and 2nd type1«<
-SSS: Sick sinus syndrome
-Sinus Bradycardia (lightheaded, ringing in ears)» if serious s/s, start transcutaneous pacing
***systolic murmur: mitral regurg secondary to papillary muscle rupture = loud holosystolic murmur at apex (MCL 5th ICS) that radiates to axilla (anxious, diaphoretic, hypotensive)
> > > RV infarct and posterior MI associated w/ inferior MI
-s/s: high CVP, JVD at 45 degrees, clear lungs, bradyarrhytmias, STE in V4R
-30% of inferior MI have RV infarct; want to avoid nitrates and diuretics, caution w/ BB –> GIVE FLUIDS AND POSITIVE INOTROPES
Anterior MI
V1-V4 (SEPTAL V1-V2)
(reciprocal in inferior II, III, aVF) - ST depression
LAD occlusion (Left anterior descending)
**Associated w/ common bundle of his disturbances:
-2nd Type II AVB (remember A22)
-RBBB
»94% mortality, need pacemaker
***Systolic murmur: VSD (heard lower L sternal border 5th ICS)
> > > higher mortality for HEART FAILURE than inferior
Lateral MI
I, aVL (high lateral)
V5, V6 (low lateral)
Left circumflex artery occlussion
Most common complication of MI
arrhythmias
- defib VF
- Stable sustained VT, drug therapy
- unstable sustained VT, cardiovert
PAD: s/s (the 6 “Ps”)
- Pain (activity, rest)
- Pallor
- Pulse absent or diminished
- Paresthesia
- Paralysis
- Poikilothermia: loss of hair on toes or lower legs; glossy, think, cool, dry skin (chronic sign)
Additionally, cool to touch, minimal edema
Regarding perfusion, don’t elevate extremity, put bed in reverse Trendelenburg
Ankle-brachial Index (ABI).
What is normal?
assess for PAD
Normal is > 0.90
Divide ankle pressure by brachial pressure on same side
Dilated Cardiomyopathy
LV enlarged, thinning wall, dilated and issue with ejecting blood thus decreasing contractility and causing compensatory arterial constriction
SYSTOLIC HEART FAILURE
–MV regurg occurs d/t the ventricle dilation
> > > GOAL: increase contractility, decrease preload and decrease afterload (arterial constriction)
What causes a prolonged QT? What can this lead to?
Normal is 0.32-0.44
Electrolytes: low K, Ca, or Mg
Drugs: Amiodarone, Quinidine, Haloperidol, Procainamide
Leads to Torsades de Pointes (Polymorphic VT)
tx w/ Mag
Dressler’s Syndrome
Dressler’s syndrome usually occurs within two to six weeks after heart surgery or a heart attack, but it can take up to several months for symptoms to develop. When the pericardium becomes inflamed, it can rub against the heart and cause chest pain»_space;> SECONDARY PERICARDITIS
S/S: CP, fever, pain worse with inspiration, relief w/ leaning forward; hear a pericardial friction rub
Global STE and PR depression (frown face)
Watch for cardiac tamponade
What does a loud systolic murmur at the apex of the heart indicate?
Mitral valve regurgitation
Pacemaker settings?
- paced
- sensed
- response to sensing (Inhibits or Dual {inhibit & triggers})
Pacemake malfunctions?
- Fail to pace- no spike at all
- Failure to capture- spike, no QRS to follow for Vpaced (increase mV)
- Failure to sense- pacing in native beats (increase sensitivity)
»if pacer spike lands on T wave, need to increase sensitivity to pick up intrinsic beat. Spike on T wave can cause Tdp!
What conditions is an IABP used? How does this therapy benefit the patient?
LV heart failure, cardiogenic shock, cardiomyopathies, pts awaiting heart transplant
- benefit from decreasing afterload with deflation right before systole AT DICROTIC NOTCH
»>(D)eflate @ (D)icrotic notch «<
-increase diastolic augmentation with inflation at beginning of diastole (the coronary arteries better perfused) R WAVE OF ECG
Hypertrophic Cardiomyopathy (exam)
- thickened wall and septum inwardly at the expense of of the LV chamber so less CO, filling issue
- ventricles rigid and stiff restricting filling (decr SV&CO)
DIASTOLIC HEART FAILURE
> > Do not want to increase contractility or dilate vessels (this pools blood in periphery)!! **Instead give BB or CCB to slow heart and allow more filling time
***INCREASED RISK OF SUDDEN CARDIAC DEATH
What is HTN Emergency/Crisis?
-elevated BP > 180/120 w/ evidence of end organ damage (brain, heart, kidney, retina)
s/s: blurred vision, SOB, crackles, S3 & S4
> Accelerated HTN DBP >120
Malignant HTN DBP >140
Tx: Nitroprusside drip to decr preload and afterload (vasodilator)»_space;>reduce MAP by 25% in 2hrs, then decr 160/100 in 2-6 hrs
> > Greatest risk is stroke, need to reduce BP quick.
~~~Tyramine is an amino acid that can trigger a HTN crisis in a patient taking MAO inhibitors
–urgency is the elevated BP w/o end organ dmg»_space;oral agents ok and bring BP down in 24-48 hrs (ACE-I, CCB, Clonidine)
Cardiac tamponade s/s
-this is blood, fluid, or air in pericardial sac
BECK’S TRIAD:
- muffled heart sounds
- JVD
- Hypotension and narrowed pulse pressure 82/68
Also Pulsus paradoxus: drop in SBP >12mmHg w/ deep inspiration – cause intrathoracic pressure to increase & venous return to decrease
Dx: TTE or TEE (best b/c can see behind heart)
–can be cause PEA (pulseless electrical activity)
What medication is given for Afib rate control?
Calcium channel blockers.
D/t the loss of atrial kick, digoxin (cardiac glycosides) given to help with contraction
S3 vs S4 heart sounds
Both heard best at apex w/ bell (MCL 5th ICS)
S3 caused by:
- associated with HF, fluid overload
- pulm HTN leading to cor pulmonale (RHF)
- mitral, aortic, or tricuspid insufficiency
S3 occurs early in diastole, right after S2
»rapid rush of blood into the dilated ventricle
S3 = tennessee
________________________________________
S4 caused by:
-MI, infarction, HTN, ventricular hypertrophy and AORTIC STENOSIS
S4 occurs right before S1 (systole)
S4 = kentucky pour
» caused by atrial contraction of blood into NON-COMPLIANT ventricle (so not heard w/ Afib)
What is the difference between high and lose dose DOPAMINE?
At high doses > 10mcg/kg/min, alpha receptors are stimulated in arteries and causes vasoconstriction
At low doses < 5mcg/kg/min, beta-1 receptors in heart produce positive inotropic effect (incr contractility)
*remember chronotropic effects HR