2.2 Cardiovascular, Acute Coronary Heart Disease Flashcards
Acute Myocardial Infarction
Discuss coronary artery disease and angina pectoris
Coronary Artery Disease:
Impaired blood flow to the myocardium, usually caused by atherosclerotic plaque in the coronary arteries. Can be asymptomatic or may lead to angina pectoris, acute coronary syndrome, myocardial infarction, dysrhythmias, heart failure and death.
Angina pectoris:
Chest pain resulting from reduced coronary blood flow which causes imbalance myocardial blood supply and demand
May be due to coronary heart disease, atherosclerosis or vessel constriction
Acute Myocardial Infarction
Discuss pathophysiology of AMI
Patho AMI:
Blood flow to a portion of cardiac muscle is completely blocked, resulting in prolonged tissue ischemia and irreversible cell damage. Coronary occlusion is usually caused by ulceration or rupture of a complicated atherosclerotic lesion. When atherosclerotic lesion ruptures or ulcerates, substances are released to stimulate platelet aggregation, thrombin generation. Vessel constriction and a thrombus (clot) forms, occluding the vessel and interrupting blood flow to the myocardium
Acute Myocardial Infarction
Identify assessment findings related to AMI and ACS
Pain:
heaviness/pressure/burning/tightness
substernal or precordial; may radiate to neck, arm, jaw
indigestion, upper back pain, atypical
Skin:
ashen, cool, clammy
Cardiovascular:
Initial elevation of BP and HR but BP can drop with decrease cardiac output
Shock= reduced perfusion of organs (brain, liver, kidneys, etc)
Abnormal heart sound S3 and S4, murmurs
Nausea and vomiting
Fever:
inflammatory process caused by cell death, increased WBC
Anxiety:
impending doom or denial
Acute Myocardial Infarction
Describe the diagnostic process of ECG
ECG changes evolve over course of MI
ST depression= ischemia (inadequate blood supply)
ST elevation= injury
Q wave= infarction (obstruction of the blood supply)
T wave inversion= ischemia or injury
Ischemia: an inadequate blood supply to an organ or part of the body, especially the heart muscles
Infarction: obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue
ECG leads determine location of MI
ECG within 10 min of arrival to ER
**infarcted tissue doesn’t conduct normally
Acute Myocardial Infarction
Describe the diagnostic process of cardiac enzymes
Cardiac enzymes (markers): Proteins released when myocardial cells die, they determine the timing and severity of MI. Tests are repeated q6-8 hours for 24 hours
Myoglobin: first detectable but nonspecific with limited use (not often used)
Troponin: Elevates in 2-4 hours, peaks in 10-12 hours, return to baseline within 10 days. MOST specific indicator of MI
CKMB/CK ratio (heart specific/total body): Elevates in 4-8 hours, peaks 18-24 hours, return to baseline within 3 days.
Increased CK= muscle injury
Increased CK-MB= cardiac muscle injury
Acute Myocardial Infarction
Describe the diagnostic process of stress testing
Stress testing
When cardiac enzymes are negative a stress test is ordered
Many stable outpatients have stress tests for initial screening
Exercise testing on treadmill and monitored
Medication induced stress when a patient can not walk on treadmill (meds: Persantine, dobutamine)
Myoview: nuclear isotope tracer (thallium) injected to evaluate UPTAKE into heart muscle
-assess coronary blood flow, perfusion to the myocardium
-scanned with exercise, then repeated at rest (2-3 hrs later)
Acute Myocardial Infarction
Describe the diagnostic process of echocardiogram
Echocardiogram:
Sonographic imaging of the heart
Transthoracic (more common) or Transesophageal, requires sedation
Evaluation of cardiac anatomy and function:
Muscle function/wall motion
Muscle thickness
Valve function
Chamber size and shape
Pericardial fluid
Thrombus
**does not evaluate vessels or conduction
Acute Myocardial Infarction
Describe and give rationale for nursing and medical interventions including medications
Nursing interventions for AMI
Anticipated orders: telemetry, serial ECG serial cardiac enzymes oxygen IV access (2 IV's, 18 g) bedrest to reduce cardiac workload; BSC light diet, small frequent meals but NPO initially diagnostic testing cath lab ASAP with STEMI
Medications:
Nitro- vasodilation, reduced cardiac workload, reduced anginal pain, improves perfusion. First line!
Morphine- drug of choice is nitro is not relieving pain, reduces anxiety, reduces cardiac workload
Aspirin- prevents platelet aggregation, chew for rapid buccal absorption
Heparin- does not lyse clots, prevents further buildup of thrombus
Beta Blocker (“olol”)- reduced O2 demand by reducing HR, BP and contractility, limit size of infarct, reduce risk of reinfarction and arrhythmias. Not used in shock state
Ace Inhibitors (“pril”)- prevents ventricular remodeling and heart failure, reduces mortality
Antidysrhythmic (amiodarone)- if needed, dysrhythmias are common
Cholesterol meds- underlying atherosclerosis
Laxatives- to avoid straining with BM
Acute Myocardial Infarction
Discuss inter-professional collaboration, including providers and cardiac rehab
.
Acute Myocardial Infarction
Complications of AMI
DYSRHYTHMIAS
AMI Dysrhythmias:
Most frequent complication
Infarcted tissue is arrhythmogenic, alters impulse generation and conduction
PVC’s very common d/t ventricular irritability
Vtach and Vfib, frequent cause of sudden cardiac death, less common. Shockable rhythms
AV Blocks, common with anterior wall infarction, brady, right sided
Bradycardias, common with inferior wall infarction
Acute Myocardial Infarction
Complications of AMI
HEART FAILURE AND PULMONARY EDEMA
.
Acute Myocardial Infarction
Complications of AMI
PERICARDITIS
Pericarditis
Inflammation of pericardium: dual membrane sac, holds 30-50ml serous lubricant fluid. Inflammation may cause scarring and become chronic
Infectious causes: vial most common, heals with time
Noninfectious causes: many, including myocardial injury, autoimmune disease, cancer
Pericardial effusion: more than 50ml of fluid
Cardiac Tamponade: pressure around heart and unable to pump= decreased BP, narrow pulse pressure, muffled heart tones, JVD, anxiety, signs of shock
Assessment: Chest pain: acute and sharp, worse on inspiration and relieved with leaning forward. Pericardial friction rub Mild fever Tachycardia Increased WBC and SED rate Slight increase in cardiac enzymes
Medica management:
Tylenol for fever
NSAIDS for inflammation, steroids if needed
Treat underlying cause
Surgical management:
Pericardiocentesis: needle aspiration
Pericardial window: removal of small rectangle of the pericardium
Pericardiectomy: removal of entire pericardial sac, typically requires a sternotomy
Acute Myocardial Infarction
Complications of AMI
MITRAL VALVE DYSFUNCTION and other structural defects
Mitral Valve:
Papillary muscle rupture
-Ischemia= papillary muscle dysfunction or rupture
-Sudden valve failure, typically mitral regurgitation, loud murmur, surgery immediately
Necrotic muscle= scar tissue, stiff, noncompliant
Ventricular aneurysm= scar tissue displaces outward
Myocardial rupture
Acute Myocardial Infarction
Discuss rationale for hypothermia and nursing interventions
Hypothermia therapy:
Protects brain from cellular injury
Initiated after Vtach or Vfib arrest (when pulse is recovered but patient still unresponsive)
Goal:
Reduce metabolic rate and O2 demand
Stabilize cell membrane
Reduce ischemic damage and reperfusion injury caused by inflammation
Goal temp: 32-34 C, cold saline, cooling blankets
24 hour treatment, then gradual rewarming
Complex ICU nursing care: Ventilator- sedation and analgesia Fluid and electrolyte management Cardiac monitoring Protect skin- necrotic, bleeding, pressure Monitor for bleeding and kidney injury
Cardiac catheterization
Identify indications for right and left catheterization
Coronary angiography:
Gold standard for looking at coronary anatomy
Dye and fluoroscopy visualization
Right heart cath:
Measures pressures in right side of heart and lungs
Venous puncture typically in groin
Left heart cath:
Determine location and severity of blockages
Arterial puncture, typically wrist or groin
Ventriculogram:
Measures left ventricular function
Requires additional dye
Cardiac catheterization
Describe the procedure
.
Cardiac catheterization
Identify and give rationale for nursing interventions pre and post cath
Pre cath:
Baseline assessment
Post cath:
Neuro
Assess site:
-groin- bedrest 4-8 hrs w/ leg straight, HOB <30 degrees, worried about pseudoaneurysm (not true aneurysm but an injury to the lining of the artery where blood leaks out into the outer most layer, bulging, painful
-radial- pressure bands, no mobility restrictions
Distal circulation
Pain/symptoms
Cardiac rhythm
Restenosis (artery closes again after corrective surgery)
Reperfusion, may also cause angina (ex: foot falls asleep, tingling, pain)
Monitor CBC, BMP and I/O
Medications:
Nitrates
Calcium channel blockers (“dipine”, open arteries)
Antiplatelets (can be dual antiplatelet therapy)
Acute Coronary artery disease
Discuss the use of thrombolytics and nursing care
Thrombolytics (clot busters):
Used when there is no access to cath lab for PCI
Reperfusion is the goal
Treat and transfer to a PCI facility for angiography and PCI
Medications: Alteplase (tPA), Reteplase (rPA), Streptokinase within first 6 hours of symptoms onset
Nursing care: HOB <15 degrees, bedrest Cardiac monitoring Monitor for bleeding AVOID injections, catheter placement r/t bleeding after thrombolytic is administer (bleeding risk).
Acute Coronary artery disease:
Revascularization: Percutaneous Coronary Intervention (PCI)
Discuss the use of angioplasty and complications
Angioplasty is a procedure used to open blocked coronary arteries (balloon inflation of artery) caused by coronary artery disease. It restores blood flow to the heart muscle without open-heart surgery
Complications: Dissection- artery damage Vasospasm- artery irritation Dysrhythmias Restenosis- artery closes again CVA- stroke risk CIN- contrast induced nephropathy
Acute Coronary artery disease
Revascularization: Percutaneous Coronary Intervention (PCI)
Discuss the use of stents
Coronary stents are now used in nearly all angioplasty procedures. A stent is a tiny, expandable metal mesh coil. It is put into the newly opened area of the artery to help keep the artery from narrowing or closing again.
Complications: Dissection- artery damage Vasospasm- artery irritation Dysrhythmias Restenosis- artery closes again CVA- stroke risk CIN- contrast induced nephropathy
Acute Coronary artery disease
Revascularization: Percutaneous Coronary Intervention (PCI)
Discuss the use of atherectomy
Atherectomy remove plaque buildup from an artery. Removing this plaque allows blood to flow more freely through the artery.
An atherectomy often treats artery blockages that contain plaque — fatty substances made up of cholesterol, fats, calcium, and other substances.
Unlike an angioplasty, which moves plaque to the side of the artery, an atherectomy completely removes plaque from the artery
Complications: Dissection- artery damage Vasospasm- artery irritation Dysrhythmias Restenosis- artery closes again CVA- stroke risk CIN- contrast induced nephropathy
Coronary Artery Bypass Grafting (CABG)
Revascularization
Identify indications for CABG
CABG indications:
Complete occlusion and wire cannot pass
Multivessel disease (3 or more vessels blocked)
Left main coronary artery disease
Failed PCI stent
Severe left ventricular dysfunction, low ejection fracture
DM (prone to stents blocking back up)
Coronary Artery Bypass Grafting (CABG)
Revascularization
Describe the procedure
CABG procedure:
Place new vessels (bypass) from aorta or internal mammary artery to distal coronary arteries
Grafts (conduit): internal mammary artery (IMA), saphenous vein graft (SVG), radial artery
Sternotomy: large incision, cutting through sternum to access heart
Thoracotomy: incision on side of chest, very painful.
Cardiopulmonary Bypass (CPB) machine: provides a bloodless field for cardiac surgery. Venous blood is drained to a reservoir, oxygenated and sent back to the body using a pump, skipping heart/lungs. Sometimes pt can be off pump
Hypothermia: metabolism drops = less O2 demand
Temporary pacing wires
Chest tubes: fluid and air drainage
Invasive hemodynamic monitoring by arterial lines or central line
Coronary Artery Bypass Grafting (CABG)
Revascularization
Identify potential complications
CABG complications: Bleeding Pneumothorax Cardiac Tamponade Stroke Dysrhythmias Delirium (acute) Ileus: temporary lack of muscle contract in intestines Renal failure Infection Pneumonia
Coronary Artery Bypass Grafting (CABG)
Revascularization
Prioritize post op nursing interventions
Postop CABG:
Know what the patient had done
CBP (cardiopulmonary bipass) affects every system- inflammatory response
Monitor cardiac output
Oxygenation: vent, suction, airway, extubation, O2
Lungs not inflated during procedure (atelectasis
Acute pain
Dysrhythmias common
Temporary pacer (right atrial, left ventricular)
Strict I/O- report <30ml/hr x 2hr
Chest tube patency, output, air leaks
Labs: ABG’s, lytes, blood count, coags, renal function
Manage IV fluids
VS
Hemodynamic monitoring
Heart sounds: S3/S4, respiratory compromise
First several hours is recovery Once stable, recovery is aggressive -early mobilization -pulmonary rehab (inspirex, cough and deep breathing, flutter, ambulation, nebs) -bowel regimen -multimodal pain management -oral care TID with tooth brush -gum chewing -IPC's, SCD's -assess and manage delirium
Discuss heart transplant surgery
Heart transplant surgery:
When mechanical support is not enough
Only definitive treatment for end-stage HF
Postop care similar to CABG
Dysrhythmias common
Myocardial stunning common (initial post op HF)
Donor heart is denervated- lacks autonomic regulation, HR runs higher 90-110
Infection and rejection are major risks- antirejection meds are critical but increase infection risk
Hemodynamic monitoring
Explain the concepts of cardiac output (CO) and cardiac index (CI)
Cardiac output:
Amount of blood the heart pumps in 1 minute
Cardiac output= heart rate X stroke volume
Cardiac index:
Index for size, better indicator of cardiac performance
Cardiac output adjusted for body size of patient
Provides more meaningful data about the heart’s ability to perfuse the tissues, therefore is more accurate indicator of the effectiveness of the circulation than CO
Hemodynamic monitoring
Describe how preload, afterload and contractility influence stroke volume (SV) and cardiac output (CO)
Stroke volume includes: preload, afterload and contractility
Heart rate X stroke volume = cardiac output
Preload: amount of blood remaining in the ventricle. Preload is the end-diastolic stretch on the muscle fibers. Pressure inside the heart just before contraction. Usually volume dependent
Afterload: PRESSURE that the ventricular muscles must generate to overcome the pressure in the aorta. Afterload = resistance. Components of afterload: BP, valve compliance (stiff valves, arterial wall compliance (tight arteries)
Contractility: inherent ability of the myocardium to contract independent of preload or afterload, velocity and extent of myocardial fiber shortening; quality of the pump. Cannot be directly measured. Influences myocardial oxygen consumption: increased contractility= increased myocardial work= increase O2 consumption.
Hear rate: affected by the SNS. Autonomic reflexes trigger heart rate to compensate for changes in cardiac output. Multiple meds are chronotropic, affecting the heart rate. Increasing the heart rate increases cardiac output to the point where it interferes with ventricular filling
Hemodynamic monitoring
Discuss the hemodynamic effects of common vasoactive medications
.
Hemodynamic monitoring
Explain the rationale for invasive and noninvasive hemodynamic monitoring
Invasive Hemodynamic Monitoring (ART line):
Assess cardiovascular function in patients who are critically ill or unstable.
Main goal: to evaluate cardiac and circulatory function and the response to interventions.
Noninvasive:
Pulses, HR, BP, mentation, skin, breath sounds, neck veins. Labs: BNP, ABG, BMP, LFT, lactic acid
Invasive:
Measure pressures, flow and oxygenation in cardiovascular system
Pressure in vessel converted to electrical waveform
Parameters include: HR, arterial BP, central venous or right atrial pressure, pulmonary pressures and cardiac output
**trends are more significant than individual readings
Arterial Pressure Monitoring
Explain the significance of mean arterial pressure (MAP)
Mean arterial pressure (MAP):
Average pressure in the arterial system during systole and diastole
REFLECTS THE PERFUSION PRESSURE
Calculate MAP:
Systolic pressure + 2x diastole pressure/3
Ex: 120/80 BP
120 + 160 = 280/3 = 93
Normal: Systolic 100-119 Diastolic 60-79 MAP 70-90 <60 is hypoperfusion, not supplying O2 <40 is circulatory collapse
**DIASTOLE IS TWICE AS LONG AS SYSTOLE
Arterial Pressure Monitoring
Identify priority nursing responsibilities and rationale for Art-Lines
Dressing: tubing secure/ transparent dressing over insertion site
Immobilize: padded splint to immobilize in neutral position (wrist slightly hyper extended)
Assess: distal extremity for neurovascular assessments/changes
Complication: distal ischemia Thrombus Infection Nerve injury
Nursing care:
Assess site and distal perfusion
Flush lines
Maintain dressing and lines
**NEVER INFUSE ANYTHING THROUGH ART LINE
Arterial Pressure Monitoring
Describe Allen’s test
Allen’s test is used to evaluate ulnar circulation
Patient clench fist, apply pressure to both radial and ulnar arteries. Without releasing pressure have patient to unclench fist to relaxed position. Palm should be blanched due to lack of blood flow
Release pressure from ulnar artery to observe return of color within 7 seconds
If blood flow returns in 7-15 seconds= blood flow impaired
If blood flow returns in >15 seconds blood flow is considered inadequate and the radial artery should not be used in this hand
Invasive Lines (PAC= Pulmonary artery catheterization, CVC= Central venous pressure): complications and nursing care
Complications: CVC (central line pressure, access by jugular, clavicle) Infection (CLABSI): central line associated bloodstream infection Air emboli Insertion site: -bleeding -hematoma -pneumothorax PA (Pulmonary artery catheterization, access in mid arm) lines: -ventricular dysrhythmias -pulmonary infarction -pulmonary artery rupture -balloon rupture- emboli
Nursing care:
Verify placement by x-ray prior to infusion
Flush line to keep patent
Assess distal circulation with limb sites
Assess sites for infection, infiltration, phlebitis
Strict aseptic technique, scrub the hub
Follow protocols for dressing and tubing changes
Hold pressure when pulling
Describe the effect of heart disease of reproductive health
Oral contraception
Hormone replacement therapy
Summarize essential aspects of discharge teaching
Risk factor modifications: Smoking cessation Cardiac diet Glycemic control Weight loss
Activity guidelines: restrictions and goals
Medications ASA/Antiplatelets Beta blockers Nitrates ACE/ARB Statin Diuretics Anticoagulants Antiarrhythmics
Multidisciplinary:
RN, provider, PT/OT/ST, case manager, social work, cardiac rehab, palliative care
Assess capacity for ADL’s, mobility , medication management, wound care
Angina aggravating factors
O2 Supply: Atherosclerosis Anemia Lung disease Dysrhythmias Hypovolemia Valve disorders
O2 Demand: Exertion Cardiomyopathy Tachycardia Hypertension Hyperthermia Stress
**Myocardial ischemia: insufficient O2 supply= cardiac chest pain
Impaired Coronary Perfusion
Coronary artery occlusion with stable plaque
Platelet aggregation forms a thrombus
Coronary vasospasm (Printzmetal’s angina)
Drop in BP= reduced coronary perfusion pressure
Autoregulatory systems fail
Acute Coronary Syndrome (ACS)
Spectrum of myocardial ischemia- injury- infarction- necrosis
Not getting enough O2 to heart muscle, supply and demand is off balance
Most often due to atherosclerosis
Unstable angina
Acute myocardial infarction (AMI)
-NSTEMI (non ST elevation myocardial infarction)
-STEMI (ST elevation myocardial infarction)
Cardiac Diagnostics Additional Labs
CBC- increased WBC r/t inflammation and damaged muscle
PT/PTT- baselines before intervention
BMP- electrolytes and renal function
Liver Function Test
ABG’s- oxygenation and acid/base balance
Assess risk factors: lipid profile, Hgb A1C
Define: Unstable angina NSTEMI STEMI Necrosis
Time is muscle. Damage begins within 30 minutes
Unstable angina- ischemia: partially occluding thrombus
NSTEMI- injury (not full thickness): T wave inverted or ST depressed, enzymes positive, platelet aggregation, early thrombus
STEMI- infarction (full thickness): Elevated ST segment, may have Q wave, thrombin rich thrombus, conduction problems can cause life threatening dysrhythmias
Necrosis- permanent damage
**GOAL: restore blood flow, treat dysrhythmias, stabilize
MONA
Morphine: relieves pain, decreases workload
O2: keep stats >92%
Nitroglycerin: relieves pain, dilates arteries and veins, improves coronary perfusion, reduces workload (usually given first)
Aspirin: platelet inhibitor
Quality: Core Measures for ACS
On arrival:
Aspirin
ECG
Time to PCI or fibrinolytics:
90 min CMS mandate for STEMI
Smoking cessation counseling
At discharge: Statin Beta Blockers Aspirin ACE/ARB with MI, DM, CHF
AMI Complication: Infarct Extensions
Extension of the original infarct
Presents with same s/s as original MI
Typically seen 10-14 days after MI
Risks is minimized by medication:
Aspirin
Beta blockers ("olol")
ACE ("pril") inhibitors or ARB ("sartan")
Revascularization proceduresAMI complication: encephalopathy
Encephalopathy:
Neurologic injury following cardiac arrest
Arrest survivors- high risk for hypoxic brain injury and permanent neuro deficits
Statistics- up to 80% are comatose, 10-30% have “meaningful neurologic recovery
Oxygen and ATP stores that “feed” the brain are used up in about 5 minutes
Prevention:
Excellent CPR- push hard, push fast
Early defibrillation
Targeted temperature management or therapeutic hypothermia
AMI complications: Pump failure
Pump Failure:
Acute heart failure from muscle wall injury
Severity dep on location and size of MI
Cardiogenic shock- cardiac output cannot meet O2 demands and organs begin to fail
Left HF:
Large anterior MI (LV)
S/S: crackles, dyspnea, frothy cough, S3 gallop, mentation changes, cough
Right HF:
Large inferior MI (RV)
S/S: JVD, ascites, peripheral edema, hypotension
Heart Failure classifications
HF classifications:
Acute vs Chronic:
Refers to onset and current ability to compensate
Left vs Right:
One always leads to the other over time
Systolic vs Diastolic:
Systolic- disease of pumping
Diastolic- disease of filling
Low output vs High output:
Low- cardiac disorder with increased cardiac output
High- increased metabolism, cardiac output can’t meet demands: hyperthyroidism, sepsis
Heart Failure: nursing care
Monitoring:
Labs- BNP, renal, lytes, weights, I/O, BP, HR, breath sounds
Education:
Meds, diet, daily weights, activity/rests balance, when to call, follow up appointments
Medication:
Beta blockers (“olol”)- reduce O2 demand, workload, HR and BP
ACE (“pril”)/ARB (“sartan”)- vasodilation, reduce O2 demand, workload, remodeling, cardiomyopathy
Entresto- combo of ARB and sacubitril, increase natriuretic peptides
Diuretics
What are hemodynamics?
Blood movement
Study of blood flow or circulation
Management of volumes and pressures to optimize the delivery of oxygen to all the cells of the body
REMEMBER THE CELL The end goal is NOT blood pressure Goal is cellular respiration Cellular respiration is the foundation for life Focus on oxygen delivery to the cell
Preload Assessment
RIGHT AND LEFT
Right:
Central Venous Pressure (CVP)
Noninvasive- JVD, peripheral edema, weight
Left:
Pulmonary Capillary Wedge Pressure (PCWP)
Noninvasive- lung sounds, BP, urine output (low), weight
Afterload Assessment
RIGHT AND LEFT
Right:
Pulmonary vascular resistance (PVR)
Elevated PVR = pulmonary hypertension
Left:
Systemic vascular resistance (SVR)
Noninvasive- diastolic blood pressure
Arterial Pressure Monitoring with ART LINE?
Direct, continuous monitoring of systolic, diastolic and mean arterial pressure
Easy access for arterial blood samples and ABG’s
Assess blood volume and response to vasoactive meds
Most common placement is radial (femoral and brachial also used)
Before placement, check Allen’s test
What is Central Venous Catheter (CVC) and Central Venous Pressure (CVP)
Central Venous Catheter (CVC):
Venous access and monitoring central venous pressure
Multiple types of CVC access, not all monitor CVP
Most common is triple lumen, can read CVP
-most common, subclavian, internal jugular, femoral
-femoral CVC are not accurate but are useful for trending
Purple Power PICCS can be used for CVP monitoring
Ports are NEVER used for CVP monitoring
Central Venous Pressure (CVP): Pressure in right atrium- ASSESS preload Assesses venous return to the heart- think volume Normal CVP value- 2-6 mmHg (higher in sick people) Increased CVP: -right sided heart failure -volume overload -pulmonary hypertension -cardiac tamponade Decreased CVP: -hypovolemia -shock
What is Pulmonary Artery Catheter (PAC) and Pulmonary Artery Pressure (PAP)
Pulmonary Artery Catheter (PAC):
Placed for detailed assessment for stroke volume and management of shock status
High risk- requires meticulous care and monitoring
Venous access (right internal jugular most common)
-balloon tip “floats” through right ventricle and into pulmonary artery
-wedges in small pulmonary artery branch
-balloon is then deflated and catheter tip rest there
Calculated assessments not directly measured
-Cardiac output/index: overall pump function
-Systemic Vascular Resistance: left and right, afterload assessment, think constriction (afterload)
-Stroke Work Index: left and right, contractility assessment
Pulmonary Artery Pressure (PAP): Measured continuously by pulmonary artery catheter Normal PAP 15-30/8-15 Increased PAP -left sided heart failure -increased pulmonary arterial resistance (pulmonary HT, mitral valve disease, hypoxia) Decreased PAP -low circulating blood volume
Arterial waveform
Pulmonary Capillary Wedge Pressure (PCWP)
PCWP:
Reflects left atrial and ventricular pressures
Measured when the inflated balloon wedges in the pulmonary vasculature
Also called pulmonary artery occlusive pressure and pulmonary artery wedge pressure
High risk procedure:
Effectively creates a PE
Balloon can rupture
Can injure the artery
Increased PCWP:
Left sided heart failure
Cardiac tamponade
Decreased PCWP:
Low circulating blood volume
