Cardiovascular CCRN
What increases SVR?
volume, peripheral vasoconstriction, low CO states, hypothermia, increased blood viscosity, hypovolemia, vasopressors, LV failure, alpha-adrenergic agents
Complications of PCI
✰ Stent thrombosis is most likely to be on the test Most incidents occur acutely (within 24 hours of stent placement) or subacutely (within the first 30 days) ✰ Retroperitoneal bleed is most likely to be on the test n Coronary artery perforation n Distal coronary artery embolization n Intramural hematoma n Failure of stent deployment n Stroke or TIA: greater risk if with aortic stenosis n Arrhythmias n Renal failure
What is effect of nitroglycerin?
vasodilator (coronary arteries and systemic venous system)
What causes decreased PVR?
vasodilators, correction of hypoxia, prostaglandins, prostacyclin
What are important considerations in RV infarct?
A right-sided ECG may demonstrate the ST changes. Treatment - Fluids - Positive inotropes Avoid - Preload reducers → nitrates, diuretics - Caution with beta blockers, often cannot give initially due to hypotension
How to care for a patient with acute PAD issues?
Embolectomy, bypass graft, angioplasty ✰ Bed in reverse Trendelenburg ✰ Do NOT elevate the affected extremity—will decrease perfusion Medications - Thrombolytics (tPA) - Anticoagulants (heparin) - Antiplatelet agents (ASA, clopidogrel) - Vasodilators
How to tell generally which type of shock you are looking at based on vital signs?
* hypovolemic, cardiogenic - narrowed PP, increased HR (check the H&P, echo - does this person have a condition which would indicate potential for cardiogenic shock?) * neurogenic - widened PP, decreased HR * anaphylactic, septic - BP down, HR up
What are the effects of titration of dopamine?
2-10 mcg/kg/min = increased contractility (beta effects) >10 mcg/kg/min = vasoconstriction (alpha effects)
What are the titration rates of dobutamine?
2.5-20 mcg/kg/min
What is perfect capillary pressure? What is the pressure in the capillaries as blood transitions to venous pressure?
30 mmHg 30 mmHg to 10 mmHg
What are you looking for in vascular assmt of post-cath patient (arterial insufficiency)?
6 Ps pain, pulse, pallor, polar (cold), paresthesia, paralysis
MAP interpretations: 70-105; <60, <40
70-105: normal; <60: perfusion deficits (gut takes first hit); <40: cardiovascular collapse - nothing is perfused
Normal Mean PAOP
8-12 mmHg (although varies depending on LV function) this is the average pressure in the pulmonary circuit during systole and diastole
What is the normal ABI? What is it used for?
< 1 (divide ankle pressure by brachial pressure on the same side) used to assess for PAD
Aneurysms, location, frequency, treatment
AAA - 75% of all cv-related aneurysms thoracic AA - 25% of all cv-related aneurysms Treatment of Aneurysms n Aneurysms < 5 cm in diameter and no symptoms Monitor regularly - Ultrasound or CT scan Treat hypertension: drug class of choice is beta blockers, which may slow growth People with Marfan's syndrome are often treated sooner n Thoracic aneurysm causing symptoms or > 6 cm Surgical repair Dissection: SURGERY Aggressive treatment of hypertension and heart rate control - Labetalol drip
What are the components of blood pressure?
BP = CO x SVR
What are risks for prolonged QT and Torsades?
Causes of prolonged QT include: Drugs—amiodarone, quinidine, haloperidol, procainamide Electrolyte problems—hypokalemia, hypocalcemia, hypomagnesemia Treatment for torsades VT—magnesium
What are considerations for nipride administration?
Assess for cyanide toxicity secondary to drug metabolite (Thiocyanate): mental status change (restlessness, lethargy), tachycardia, seizure, a need for ↑ in dose, unexplained metabolic acidosis, especially in those with renal impairment or when drug is used > 24 hrs
Location and function of dopaminergic receptors
renal, mesenteric vascular beds, stimulates vasodilation
Nursing care of cath patient, pre-procedure?
NPO, consent, labs, ecg, insulin orders, oral meds for diabetics (metformin and contrast dye are BAD MIX for kidneys), prehydrate, mucomyst for renal protection / renal insufficiency pts, allergies, vascular exam on call: ASA, clopidogrel (Plavix), etc.
What are effects and indications for nicardipine (Cardene)?
CCB > vasodilation indications: htn crisis, afterload reduction infusion: 5-15 mg/hr
Cardiac Index
CO / BSA = Normal: 2.5-4.0 L/m2/min; considers body size in relation to CO, more meaningful than CO
Cardiac Output Calculation
CO = HR x Stroke Volume
What are three ecg changes you will see in MI that indicate ischemia, injury and infarction?
T wave inversion, ST segment elevation in two or more contigous leads, pathological q-wave (indicates past MI) with ST segment elevation
Oxygen consumption and delivery
DaO2 - arterial oxygen delivery: 100% SvO2 - true mixed venous O2: 60-75% VO2 - venous O2 (consumption) ScvO2 - central venous O2 in rt atrium: > 70%
Patient care following reperfusion of STEMI - Fibrinolytic Therapy
Fibrinolytic Therapy (30 minutes door to drug administration) n Absolute contraindications Any prior intracranial hemorrhage Known structural cerebral vascular lesion (e.g., arteriovenous malformation) Known malignant intracranial neoplasm (primary or metastatic) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed-head or facial trauma within 3 months ✰ Evidence of reperfusion Chest pain relief: due to fibrinolysis of clot Resolution of ST segment deviations: due to return of blood flow Marked elevation of troponin/CK-MB: due to myocardial "stunning" when vessel opens Reperfusion arrhythmias (VT, VF, accelerated idioventricular rhythm (AIVR)): due to myocardial "stunning" when vessel opens
What is a potential complication of using vasopressin in managing shock states?
vasopressin is a coronary artery constrictor, so use sparingly in people with cardiac histories
12-lead EKG - location of leads/issues
II, III, aVF - inferior wall LV, RCA V1, (V2) - anterior septal wall, LAD, RCA posterior LV V2, V3, V4 - anterior wall, LAD I, aVL,(high) V5, V6 (low) - lateral wall LV, Lt Cfx V7, V8, V9 - posterior wall (from rt side ekg)
What are two major functions of ventricular diastole?
ventricular filling, coronary artery perfusion
What are treatment options for hypertensive crisis?
Labetolol - alpha and beta blocker Metoprolol, Esmolol - beta blockers Nicardipine - ca channel blocker Nitroglycerin - nitrates
What structures are supplied by the LCA?
Left Mainstem LCfx - left atrium, high lateral left ventricle LAD - 2/3 septum, anterior left ventricle, apex
What is the difference between hypertensive urgency and crisis/emergency, and what are the treatments for crisis/emergency?
One question may be on this topic. The question is usually related to how the topic differs from hypertensive urgency or what drugs are used for treatment. n Biggest risk is STROKE n Hypertensive emergency or CRISIS is elevated B/P with evidence of end-organ damage (brain, heart, kidney, retina) that can be related to acute hypertension → need critical care admission n Hypertensive urgency is elevated B/P without evidence of acute end-organ damage → usually no need for critical care admission n Treatment of hypertensive crisis or emergency → emergent lowering of B/P needed Nitroprusside - Preload and afterload reducer -- (remember administration considerations!) Labetalol - Intermittent IV doses preferred to continuous infusion due to possibility of continuing of drug beyond maximum dose of 300 mg - Duration of effect persists 4-6 hrs after IV dose is discontinued
Patient care following reperfusion of STEMI - PCI
PCI (90 minutes, door to balloon inflation in coronary artery at point of lesion) n Monitor for signs of re-occlusion: chest pain, ST elevation → contact physician n Monitor for vasovagal reaction during sheath removal → give fluids, atropine Hypotension < 90 systolic with or without bradycardia, absence of compensatory tachycardia Associated symptoms of pallor, nausea, yawning, diaphoresis n Monitor for bleeding: sheath site Immediately apply manual pressure 2 finger breadths above the puncture site Continue manual pressure for minimum of 20 min (30 min if still on GP IIb/IIIa inhibitors) to achieve hemostasis n Monitor for bleeding: retroperitoneal → fluids, blood products Sudden hypotension Severe low back pain n Monitor for vascular complications → pulse assessments
Define afterload. How to measure?
Pressure the ventricle must generate to open semilunar valves and eject contents. LV: SVR, RV: PVR
coronary arteries
RCA, LCA > LCfx, LAD
What is a potential side effect of ace inhibitors?
angioedema / cough
What do S3 and S4 heart sounds signify? What do all heart sounds signify and where are they best heard?
S4: myocardium is non-compliant/stiff; loudest at apex with bell. (ischemia, infarct, htn, vent hypertrophy, aortic stenosis) S1: ventricular systole (mitral/tricuspid shut); loudest at apex S2: ventricular diastole (aortic/pulmonic shut); loudest at base, louder with PE S3: volume overload - too much volume in ventricle; loudest at apex with bell. (HF, pulm htn, cor pulmonale *rt side HF, insufficiency)
What are the key hemodynamic factors?
SvO2, CO/CI, Hgb/Hct, Oxygenation, Metabolic Demand >> related to SvO2
Describe the types of aortic dissections. What type of treatment is expected?
Type A - surgical emergency, treat with stent if possible. After surgery, special emphasis on htn. Monitor spinal fluid pressures, goal < 8-10 mmHg, drain fluid to maintain. Neuro assmts, peripheral and central. Type B - treat medically if possible; reduce lt ventricular contractility and velocity of blood flow, reduce SBP to no higher than 120 relief of pain is most important clinical sign; vigilant monitoring of BP
Preload (definition and assessment)
Volume of blood in the ventricle at the end of diastole. Assmt: RV - CVP, RA pressure LV - PAOP / PAD / LA pressure
expected angina / CAD management
antiplatelet therapy vasodilator beta blocker ace inhibitor statin
S/S of acute aortic dissection
ascending aorta: chest pain, aortic insufficiency, CHF transverse aorta: dyspnea, stridor, hoarseness, cough, chest pain, JVD descending aorta: back or chest pain
What does cardiac tamponade look like from a PA cath? What are other signs?
all pressures go up and start to equalize narrowed PP Pulsus paradoxus: excessive drop in SBP (>12 mmHg) during inspiration. Cardiac muscle restriction due to tamponade, with inspiration, intrathoracic pressure increases, decreases venous return. Electrical alternans - electricity alters direction Beck's Triad - hypotension, JVD, distant heart sounds
Why are beta blockers important for patients with HF?
vfib/vtach are the most common causes of death in these patients, and beta blockers are the only class of drugs that have been shown to reduce sudden cardiac death d/t these two reasons
What increases MAP?
volume infusions, peripheral vasoconstriction, increased contractility, hypervolemia, vasopressors
What are the effects of titration of epinephrine?
lower rates, 0.005-0.02 mcg/kg/min = beta stimulation; increased HR, inotropic effects, vasodilation higher rates alpha stimulation = increased SVR, increased BP and renal artery vasoconstriction, bronchodilation
What is the CO/CI definition of cardiogenic shock?
marked decrease in CO, CI = < 1.8 L/m/m2
Nursing care for aortic dissection.
control BP repair: stent or surgical postop care: pain control, BP control (usually 140-160 SBP), pulmonary concerns, renal concerns (because a lot of dye is used during stent placement), ambulate, incentive spirometer
What is a concern for a patient who is on nipride? What lab value can be monitored for this concern?
cyanide toxicity lactic acid
What structures are supplied by the RCA?
right atrium, right ventricle, posterior left ventricle (left ventricular inferior wall), SA node, AV node, top of septum with bundle
Nursing care of cath patient, post-procedure?
monitor ecg, vascular assmt, activity restriction / progression, sheath removal, labs: heparin protocol, IIb IIIa infusion look for narrow PP for indication of retroperitoneal bleed or hidden bleed
How does the IABP improve coronary blood flow?
decreases afterload, increases coronary perfusion
What are coronary arteries dependent on for filling?
diastolic time diastolic BP (DBP)
What are three types of cardiomyopathy?
dilated: most common causes: CAD, viral, chemo, pregnancy, parasitic, alcohol hypertrophic / obstructive: causes: aortic stenosis, congenital restrictive: causes: infiltrative diseases
What decreases MAP?
diuretics, peripheral vasodilation, inotropic therapy, hypovolemia, vasodilators
What decreases SVR?
diuretics, vasodilators, hyperdynamic phase of sepsis, peripheral vasodilation, loss of vasomotor tone
Complications of AMI
dysrhythmias, HF, cardiogenic shock, papillary muscle dysfunction or rupture (heard at apex), ventricular septal defect (systolic murmur, heart at tricuspid), cardiac rupture, ventricular aneurysm, pericarditis, sudden death
In general, what is the goal of critical care?
enhance O2 delivery and decrease O2 demand SUPPLY vs. DEMAND
What are the effects of neosynephrine?
pure alpha stimulator, primarily vascular > increase SBP, increase DBP, increase PAP, coronary and renal vasoconstriction indirectly releases norepinephrine from storage sites * can cause reflex bradycardia
What affects PAOP (high and low)?
high: LV failure, valvular heart disease, cardiac tamponade; low: hypovolemia?
What typically causes low pulmonary pressures?
hypovolemia
What causes increased PVR?
hypoxia, pulmonary edema, ARDS, PE, heart defects, PEEP, pulm htn, sepsis, valvular heart disease
What is an important consideration in bradyarrythmias?
if atrial kick is not intact (ventricular rhythms, for example), consider the impact of blood filling property to the ventricles
How can you manage preload in a patient pharmacologically?
if their kidneys are working, you can try diuretics (lasix, bumex) if not, try vasodilators (nitro, natrecor)
What are three drugs that you would anticipate giving in acute decompensated HF?
impact >> preload: monitor volume (low Na diet), diuretics, NTG, ace inhibitors, pulmonary vasodilators, IABP afterload: beta blockers (not in acute SysHF) contractility: IABP, inotropes (not in acute SysHF)
Effects of Beta 1 receptor stimulation
increase HR, increase contractility, inotropic
What is expected treatment for ACS?
increase O2 supply, decrease demand ASA, beta blocker, heparin, NTG, morphine, GP IIb-IIIa inhibitor drugs
How can you manage stroke volume in a patient pharmacologically?
inotropes: milrinone, dobutamine, digoxin (the only PO option), dopamine
What types of dysrythmias are expected in an inferior wall MI? In a 12-lead EKG, which leads are identified?
leads II, III, aVf (what structures are supplied by the RCA, which feeds the left ventricular inferior wall?) bradycardias and heart block > why? because RCA supplies this area Associated with AV conduction disturbances: 2nd-degree Type I, 3rd-degree heart block, sick sinus syndrome (SSS), and sinus bradycardia Development of systolic murmur: mitral valve regurgitation (MVR) secondary to papillary muscle rupture (Posterior papillary muscle-tethering distance is significantly greater in inferior compared with anterior myocardial infarction.) Tachycardia associated with inferior MI → higher mortality Also associated with RV infarct and posterior MI Use beta blockers and NTG with CAUTION ***
How to administer milrinone?
loading dose 50 mcg/kg untiluted over 10 minutes infusion, start at 0.5 mcg/kg/min and increase in 0.375 mcg/kg max infusion to 0.75 mcg/kg/min
What are the titration rates of norepinephrine?
low doses - beta stimulation high doses - alpha stimulation
How can you manage (high) afterload in a patient pharmacologically? (Mgt of HF)
nipride A, B, Cs *A - ace inhibitors (-pril), angiotensin receptor blockers (-sartan), alpha antagonist (hydralazine, cardura) *B - beta blockers *C - CCBs (norvasc, nicardipine)
What is an important consideration in the administration of nitrates?
nitrate tolerance 12 hour window of free time is important
What is a normal pulse pressure? What does the pulse pressure indicate?
normal pp is about 40 and generally indicates cardiac index narrow pp = hypovolemia, drop in CO widening pp = neurogenic shock, increased ICP
What is the most available pulmonary vasodilator available for use?
oxygen
What do you expect with ST elevation in all 12 leads?
pericarditis
What is the antidote to use for infiltration of levophed?
phentolamine mesylate (Regitine), to block intense vasoconstriction
What drugs MUST be run through a central line?
potent vasoconstrictors: dopamine, norepinephrine....
What is stroke volume? Normal?
preload (volume), afterload ( right PVR / left SVR), contractility; 50-100 ml/beat
How can you manage (low) afterload in a patient pharmacologically?
pressors: norepinephrine, vasopressin, neosynephrine (levo, vaso, neo) also high dose epi, high dose dopamine,
Acute management of STEMI
same as acute chest pain: stat ecg read in 10 minutes n Aspirin Chew, give ASAP, improves morbidity/mortality n ANTICOAGULANT: heparin or enoxaparin n Antiplatelet agents Clopidogrel (Plavix) Abciximab (Reopro) Eptifibatide (Integrilin) Tirofiban (Aggrastat) n Beta blocker Unless ACS due to cocaine Use cardioselective such as metoprolol, do not use non-cardioselective such as propranolol Contraindications include hypotension, bradycardia, use of phosphodiesteraseinhibitor drugs such as sildenafil (Viagra) n Treat pain Nitroglycerin Morphine n History, risk factor assessment Lab assessment Cardiac biomarkers, lipid profile, CBC, electrolytes, BUN, creatinine, magnesium, PT, PTT PLUS n Determine onset of infarct, if symptoms < 12 hours → REPERFUSION Percutaneous coronary intervention, PCI (door to balloon 90 min) Fibrinolytic drug therapy (door to drug < 30 min) n Eligibility criteria ST elevation in 2 or > contiguous leads, or new onset left bundle branch block (LBBB) Onset of chest pain < 12 hours Chest pain of 30 minutes in duration Chest pain unresponsive to sublingual (SL) nitroglycerin (NTG)
When adenosine is administered, what rhythm are you prepared for?
sinus pause (NOT asystole)
Management of acute chest pain.
stat ecg read in 10 minutes n Aspirin Chew, give ASAP, improves morbidity/mortality n ANTICOAGULANT: heparin or enoxaparin n Antiplatelet agents Clopidogrel (Plavix) Abciximab (Reopro) Eptifibatide (Integrilin) Tirofiban (Aggrastat) n Beta blocker Unless ACS due to cocaine Use cardioselective such as metoprolol, do not use non-cardioselective such as propranolol Contraindications include hypotension, bradycardia, use of phosphodiesteraseinhibitor drugs such as sildenafil (Viagra) n Treat pain Nitroglycerin Morphine n History, risk factor assessment Lab assessment Cardiac biomarkers, lipid profile, CBC, electrolytes, BUN, creatinine, magnesium, PT, PTT Integrillin (covers platelet like a blanket, preventing aggregation)
general reasons for increased HR
sympathetic response OR tissue hypoxia
general reason for increased RR
sympathetic response OR tissue hypoxia OR metabolic (lactic) acidosis
What is the primary difference between systolic and diastolic HF? Dilated and hypertrophic cardiomyopathy?
systolic = problem with ejection (EF <= 40%) diastolic = problem with filling (EF > 50%)
What two types of HF are there, and how do they present?
systolic dysfunction: problem with ejection, falling CO, low filling pressures diastolic dysfunction: problems with ventricular filling, high filling pressures, pulmonary congestion
What types of dysrythmias are expected in an anterior wall MI?
tachy dysrhythmias - vtach, vfib 2nd degree Type II, RBBB >> ominous sign possible ventricular septal defect
If a pt is rushed to cath lab without ability to get written consent, what do you do?
this is implied consent
physiologic reason for increased RR
tissue hypoxia OR metabolic (lactic) acidosis
True vs. False aortic dissection
true: all layers involved false: partial or complete disruption of aortic wall with blood contained within the adventitial layer
Treatment for nitro headache?
tylenol and cold packs
What is variant or Printzmetal's angina?
type of unstable angina associated with transient ST elevation d/t coronary artery spasm with or without lesions occurs at rest and may be cyclic, brought on by specific factors (nicotine, etoh, cocaine) negative troponin ntg resolves tx with Ca channel blockers
What is acute coronary syndrome?
unstable angina / NSTEMI
Effects of Beta 2 receptor stimulation
vasodilation, bronchodilation
Post-op Care of post CABG pt, related post-op chest tube management
✰ Tamponade ✰ Pericarditis - assess hemodynamic stability: infusions, IABP, electrolytes - cardiac arrhythmias, ventilatory status: ABG, early extubation protocol (if appropriate) - pain control, incisional care, activity progression early complications: coagulopathies (excessive bleeding, cardiac tamponade), monitor electrolytes, respiratory failure / atelectasis, renal insufficiency / ATN, cardiogenic shock, stroke ✰ Post-Op Chest Tube Management n Maintain patency. Do not allow dependent loops. Milking or stripping chest tubes is not routinely indicated. - If clots appear, gently milk chest tubes. n Mediastinal tubes remove serosanguinous fluid from the operative site; whereas pleural chest tubes remove air, blood, or serous fluid from the pleural space. n Keep chest tubes lower than patient's chest. n Do not clamp the system unless changing the drainage system or there is a system disconnect. When the tube is clamped, the connection to the negative chamber is lost. n Chest tube output >100 mL for 2 consecutive hours. Maintain hemodynamic stability Correct volume status Administer blood products
