CCRN- Cardiac Flashcards
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
What do SBP and DBP indirectly measure?
SBP - measure of CO and SV
> if a drop occurs, hypovolemia and drop in CO
DBP - measure of SVR
>if a drop occurs, vasodilation cause drop in SVR, seen with sepsis and septic shock
NSTEMI tx
diagnostic cath w/in 24hrs w/ high risk score or continued CP, signs of instability
Start GPIIb/IIIa inhibitors (Integrilin, Reopro)
Wolfe Parkinson White Syndrome
- abnormal conduction pathway allows reentrant tachycardia pathway to bypass the normal AV conduction pathway –> SVT
- will see delta wave: slow upstroke of QRS
-S/s of SVT: palpitations, dizzy, CP, SOB, syncope
»If patient unstable, cardiovert or give adensosine; patient needs ablation
**If wide QRS, may be pre-excited Afib» treated differently! Give BB, amiodarone or procanimide IV
(giving CCB, adenosine or Digoxin for pre-excited Afib will enhance conduction and lead to VF)
Tx for Systolic Heart Failure
- give BB to prevent effects of Norepi (prevent vasoconstriction)
- give ACE-I (prevent Angiotensin I from convert to Angiotensin II which cause more vasoconstriction) or ARB (prevent Angiotensin II
- K sparing diuretics to prevent aldosterone release (which holds on to sodium and water)
> > Vasoconstriction and Na/H2O retention cause ventricular remodeling (hypertrophy, dilation, apoptosis)
AHA HF Classifications
Stage A- high risk, no dysfxn
Stage B- Heart disorder or structural defect, NO symptoms
Stage C- Heart disorder or structural defect WITH symptoms
Stage D- End-stage cardiac disease, w/ symptoms despite maximal therapy (inotropic or mechanical support)
NYHA HF Classifications
Class I- ordinary activity, no symptoms; Extraordinary activity results in HF symptoms
Class II- Comfortable at rest, ordinary activity results in HF symptoms
Class III- Comfortable at rest, minimal activity results in HF symptoms
Class IV- Symptoms of HF at rest, severe limitation with physical activity
Mechanical valve vs Biological valve
Mechanical lasts longer, but requires life long anticoagulation
Biological wears down with high pressure, only short term anticoagulation but requires lifelong ASA
TAVR
Transcatheter aortic valve replacement (TAVR) is a minimally invasive procedure to replace a narrowed aortic valve that fails to open properly (aortic valve stenosis).
If too high risk for open heart
Requires DAPT: ASA for life and Clopidigrel 75mg/d for 3-6mo
Abdominal vs Thoracic aneurysms, and treatments?
Abdominal: 75%
>pulsation in ABD or low back pain, N/V, shock
Thoracic: 25%
>SUDDEN TEARING, RIPPING CHEST PAIN that radiates to neck, shoulder, back
>cough, hoarseness, dyspnea, dysphagia
**If < 5cm just monitor regularly w/ US or CT
**If > 6m need surgical repair; aggressively treat HTN and HR control with Labetalol drip
DISSECTION IS EMERGENCY SURGERY
PA Catheter
-gives systolic and diastolic
-systolic is RV squeeze blood in Pulm artery
»>elevated with any lung problem
*Pulmonary HTN
*Hypoxia
*COPD, ARDS, PE
-diastolic pulmonic valve closed, thus reflects LVEDP >>>elevated with heart problems *cardiac tamponade *LV failure *MV disease
Normal PAP is 25/10 (“quarter/dime”) or
(PAS 20-30/ PAD 6-12)
PAWP is 1-4mmHg lower than PAP (never higher!!!) So PAWP norm is 8-12 mmHg
> > > PAOP is an indirect measure of LAP which is reflective of LV preload and therefore LVEDP
**LV failure or fluid overload leads to an increase in PAOP
a wave = atrial contraction (after QRS)
Dicrotic notch = closure of pulmonic valve
c wave = MV closing
v wave = atrial filling (after T wave)
What is Ashman phenonmenon?
a long R-R followed by short R-R
Most commonly seen with Afib
Is the PAD always an accurate measure of LVEDP?
NO.
Not with RBBB.
Not w/ MV stenosis.
Not w/ MV insuffi/regurg (Large V waves on PAOP)
Not w/ Pulm HTN
Not w/ decreased LV compliance
Not w/ aortic insufficiency or pulmonic insufficiency
Cardiogenic shock
**MOST OFTEN FROM MI!!!
Compensatory:
Initially decr in CO, SNS compensates and adrenaline released which incr HR, BP, releases ADH to retain water an vasocontriction. Tachycardic, cool, pale, decr UOP
Progesses to acidosis from vasocontriction, causing vasodilation which decr CO and BP causing hypotension (decr CVP, PCWP, CO and incr SVR). The patient is obtunded and stuporous from hypovolemic shock.
REPLACE VOLUME: CRYSTALOIDS, FFP, BLOOD, COLLOIDS
CVP in relation to JVD
If JVD is 10cm above the sternal angle, just at 5cm to get CVP. So 15cm H2O.
Normal CVP 3-8
What is a difference in BP of both arms an indication of
Acute aortic dissection
Aortic valve replacement needs rhythm monitoring for?
AV block may develop due to edema, inflammation, hemorrhage, or suturing near the node
> > monitor for: 2nd degree type II
Oxygen delivery in the body
SaO2- arterial O2 saturation
»most accurate for amount of O2 in blood = DO2 (oxygen delivery)
PaO2- represents only 3% that is dissolved in plasma
SvO2- venous O2 saturation
»represents O2 reserve, it’s what’s left over after the tissues have extracted what they need
What represents the AV node delay
PR segment (not PR interval, that is atrial repolarization to ventricle depolarization)
Which part of heart is greatest risk with myocardial contusion?
Right ventricle, it’s the most anterior and behind sternum
