Cardiovascular II
Acute Coronary Syndrome
Management of Acute Coronary Syndrome THROMBINS2
▪Thienopyridines
▪Heparin/enoxaparin
▪Renin–angiotensin system blockers
▪Oxygen
▪Morphine
▪Beta blocker
▪Intervention
▪Nitroglycerin
▪Statin/salicylate
ED with Chest Pain
(Rule out MI)
Treatment (Use Acronym – MONA)
M- _________________*
O- _________________*
N- _________________
A- _________________
EKG
Cardiac enzymes
Diagnostic Cath Lab/ Interventional Cath
Angina
Progressive Disease
O2 demand > O2 supply → Myocardial Ischemia
Angina = Reversible Ischemia
Occurs when arteries are blocked 75% or more
Hypoxic within 10 seconds of occlusion
Viable for 20 minutes, then we see necrosis (MI)
Myocardial Infarction
_________________become irreversible and necrosis/ _______________ results.
Cardiac cells can withstand ischemia for approximately 20 min before death.
Earliest tissue to become ischemic is the sub-endocardium (_____________ layer).
Takes 4-6 hours for entire thickness of heart muscle to become necrotic.
______ of all MI’s are thrombus related.
Acute Myocardial Infarction – STEMI vs Non-STEMI
__________ - diseased vessel totally occluded by thrombus
_______ - diseased vessel partially occluded by thrombus
Clinical Manifestations of MI
Lack of oxygen and glucose leads to anaerobic metabolism
Lactic acid irritates nerve fibers → ________ in cardiac nerves
___________________ from transmission to the upper thoracic posterior nerve roots
Clinical Manifestations of MI
▪Pain
▪Nausea and Vomiting
▪Sympathetic stimulation
▪Fever
▪Cardiovascular dysfunction
Clinical Manifestations of MI
▪__________________ will stop in the area of cardiac cellular death
▪Degree of altered function depends on _______and______________________
▪most MI’s involve Lt. ventricle)
▪Infarctions described by area which correlates with the circulation (anterior, inferior, lateral,
septal, posterior etc.…)
▪Working to reverse occlusion and REPERFUSE and restore 02 to the tissues A.S.A.P.
Clinical Manifestations of MI - Healing
▪___________________________________ within ____ hours & enzymes are leaked from the
dead cardiac cells.
▪Proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by ___ days
→ thin wall. collagen matrix laid down.
▪Collateral circulation develops around infarcted area
▪_______________days post-MI - scar tissue is still weak -- myocardium especially vulnerable to
stress
▪_____________ - scar tissue is said to be healed
▪Scarred area:
Muscle is less compliant/uncoordinated wall motion
Ventricular dysfunction and/or
Pump failure can result
Complications of MI
Dysrhythmias –very common
HF – damage causes permanent pump failure
Pericarditis- inflammation of the 2 layered sac can lead to cardiac tamponade.
Other serious complications: Cardiogenic shock
Papillary muscle rupture, ventricular aneurysm
(covered in NURS 460)
Diagnosis of MI
12-lead ECG
Enzymes
Troponin I
C reactive protein
CK-MB (CK2)
Cath Lab- coronary angiography to identify blockage
Management of MI
ICU/CCU
▪VS/ assessment/ cardiac monitor
▪Bedrest
▪arterial catheter – continuous BP readings
After……….. cardiac cath lab for
“REPERFUSION Therapy “ to restore 02 supply!
( _____________or ______________ Therapy)
Emergent PCI
▪Cath lab with Coronary angiography to visualize blockage
▪Balloon angioplasty- catheter with balloon tip, thread past blockage, inflate and compress plaque/blockage
against the vessel wall, see reperfusion with blood and 02 now passing through. ( Fig 33.6 and 33.7)
▪Stent – sits in vessel and acts as a straw or patent venue for blood flow and 02 delivery.
▪Patients have antiplatelet therapy post-stent
( page 714)
Coronary angiography
( A:identify blockage B: place stent)
Management of MI cont.
▪Fibrinolytic Therapy (“clot busting” )
▪rPA tPA ( recombinant tissue plasminogen activator) Only administered IV.
▪Contraindications ( see 33-15 p 724)
▪ active internal bleeding
▪History of intracranial hemorrhage
▪Intracranial or intraspinal surgery, recent
▪Recent ischemic stroke ( within past 3 mos.)
▪Severe, uncontrolled hypertension
▪Significant closed head injury or facial trauma
▪Suspected aortic dissection
▪No prior treatment with streptokinase within past 6 months
*IV Heparin drips also used alongside to prevent reocculsion
CABG- Coronary Artery Bypass Grafting
(coronary surgical revascularization)
▪What is it?
1. _________________________ of ________________ for blood transport between ___________ and
_________________________
2. allows for blood flow _____________beyond the stenosis
3. an artery is stenotic if its diameter is narrowed by more than
_________________________
4. Requires sternotomy and use of
cardiopulmonary bypass (CPB) machine.
CABG graft illustration
▪This illustration shows a heart with a saphenous vein graft. The surgeon connects the vein to the aorta
(upper left) and to the coronary artery at the (lower right)
How is it done?
__________ from the saphenous vein
▪vessel is _________________
▪anastomosed (attached/sewn)__________
to aorta and distally to the blockage.
▪Re-occlusion can occur
▪venous graphs tend to develop _______________
▪life expectancy of a venous graph- not as durable as arteries
▪ASA and statin therapy
Internal Mammary Artery (IMA)
▪Left IMA is ____________________to its point of origin from the left subclavian artery,
__________________ from chest wall and ___________________ to the coronary artery to the
stenosis
▪Right ______ can be used in a similar way
▪patency rate is ____________at 10 yr post procedure
Repeat CABG (gastroepiploic artery or epigstric artery)
▪Requires a ______________________ and _____________
▪wound complications ________________
▪other arteries tend to be more delicate
▪morbidity and mortality
▪nursing care: ____large surgical sites, assess for cardiac distress thru pain, arrhythmias, and complications
such as_______or drop in blood pressure, urinary output, change in pulses
MID-CABG OP-CABG
▪MID CABG
▪Minimally Invasive Direct -coronary artery bypass graft
▪uses a thoracotomy approach to mobilize the LIMA or the RIMA using beta blockers
▪before closure, meds are stopped
▪shorter recovery period
▪Visualization is not as good as open approach with obesity interfering.
▪OFF PUMP CABG
▪Open heart surgery without use of the CPBM
▪The surgeon is working on a eating heart using mechanical stabilizers.
Cardiopulmonary Bypass Machine
▪machine receives blood from the catheters in the vena cava or right atrium, oxygenates and returns via
pump to aorta
Management of cardiopulmonary bypass
1. Allows work on a ______________
2. machine pumps oxygenated blood
3. machine receives blood from the catheters in the vena cava or right atrium, _______________________ and
returns it via pump to aorta to perfuse the organs .
4. hypothermia is created
5. the longer the machine time, higher the chance of complications
Management of a CABG
▪Pre-op IV, antibiotics
▪procedures – general anesthesia, beta blockers, crack chest, CPB, grafting , closure,
sternal drains placed
▪post op complications:
▪hypovolemia --MI or CVA
▪cardiac tamponade -- wound infection
▪arrhythmia -- hemorrhage
▪emboli
▪fever
Nursing management of MI patients
▪Acute care
▪ cardiac monitor -- rest / comfort/02
▪pain control -- anxiety control
▪Chronic care
▪ cardiac rehabilitation
▪Risk of post- op depression
(see patient education in text
▪resumption of sexual activity, exercise, etc.)
Drug Therapy
Chronic Stable Angina and ACS ( T.33-12 p 713)
ACE I’s- block conversion of angiotensin I to II
Antiplatelet aggregates- ASA, Plavix
Nitrates ( nitroglycerin) dilate coronary and peripheral vessels ↓ afterload, and ↓preload
Beta Blockers- block beta receptors, decrease heart rate, lower↓ workload of heart
Calcium Channel Blockers- decrease heart rate act as vasodilators ↓heart’s workload
Opioids-Morphine Sulfate, vasodilate/pain relief
(see other classes as well-
Anticoagulants ARBs, Thrombolytics, etc)
HF
Heart Failure
Definition
A cardiovascular state in which the____________is __________________ an adequate amount of blood to meet the
metabolic needs of the tissues. Not a disease but a condition.
The heart is a ________________pump.
According to American Heart Association
(AHA) there are about 6.5 million Americans with HF projections for a 46% rise in cases by the year 2030.
HF- The most common cause of hospitalizations in patients over the age of 65.
Risk Factors for HF
HTN/Hypertensive crisis
CAD/MI
Heart disease (like Rheumatic fever, valve disorders, septal defects
Other see in textbook
Social:
DM
Smoking
Obesity, sedentary lifestyle
HF with reduced EF ( systolic)
vs HF with preserved EF ( diastolic)
Mixed HF- means you have both happening.
HFrEF/ Systolic Failure
The heart is a failing pump
Contractility is lost
Left ventricular EF ( ejection fraction) is lowered. Preload is backing up systemically. Less stroke volume SV) less
cardiac output (CO)
Normal EF- 55%- 65% volume is ejected with each beat. The remainder is healthy preload.
This number is lowered in Systolic Failure ( < 40% EF)
▪HFpEF/ Diastolic Failure
▪The ventricles are stiff/ cannot relax and fill during diastole.
▪Preserved EF means it ‘s normal, however, high filling pressures mean less stroke volume ( SV) less
cardiac output (CO).
IMPORTANT DIAGNOSTICS TO INCLUDE ON ALL HF PATHOS:
Echo – shows EF %, SV, CO
BNP – diagnostic lab >100 pg/mL
Left-Sided HF
Patho of left sided failure
▪blood backs up through the atrium to the _______
▪increased pressure causes fluid to leak out of the vessels = ___________congestion and impaired
exchange.
▪most common causes: CAD, HTN
Clinical manifestations incl :
Increased HR, crackles, s3 s4, pleural effusion,
altered mental status, restless/confused, weakness
Dyspnea, PND, frothy pink tinged sputum.
Patho of Right Sided HF
▪Weakened ventricle
▪primary cause is left sided failure,
▪Clinical Manifestations: Increased HR,
JVD, ascites, anasarca, hepatomegaly, splenomegaly, dependent edema, anorexia and GI bloating
▪Pitting Edema
▪Memorize this!!
Left sided HF “__________________”(back up into lungs)
Right sided HF “ _______________”(back up into systemically)
Cor Pulmonale = right sided failure comes
from COPD – chronic lung diseases or acutely from pulmonary embolism.
Compensatory mechanism for HF
1.Sympathetic nervous system
2.Dilation
3. renal response (RAAS)
4. Release of BNP, ANP
These all fail to help, because they work on the premise that we have a working pump. Because the heart has failed
as a pump, these worsen the problem, not help it!
▪Complications of HF
1. – refers to acute, life threatening condition- lung alveoli fill with fluid which increases
pulmonary pressures.
▪agitated, pale
▪cyanotic
▪severe dyspnea
▪wheezing, coughing, frothy, blood-tinged sputum
▪crackles
▪2. Pleural effusion
▪3. Left ventricle thrombus
▪4. hepatomegaly
▪5. Renal failure
▪Diagnostic factors for HF
1. exam
2. chest x-ray
3 12 lead _____________
4 . Hemodynamics (stroke volume, CO)
5 ECHO (looking at left ventricular ejection fraction) also cardiac cath, nuclear imaging
6. BNP (greater than _________ pg/mL), acute exacerbation.
Management of HF
▪Treat underlying cause
▪oxygen therapy and rest
▪Daily weights
▪Sodium restricted diet
▪Pharmacology
▪See table 34-7
Pharmacology for HF
▪1. Diuretics (i.e. Lasix)
▪Reduce _______ mobilize fluids
▪loop diuretics watch→ K levels
▪2. (ACE I)
▪ Reduce ____________
▪(i.e. Capoten, Vasotec, Lotensin)
3. Beta Blockers ( low dose)*
I.e. Coreg 3.25 mg po
4. (Digoxin)
▪Positive inotrope (↑contractility)
▪Negative chronotrope (↓ HR)
(Entresto, Hydralazine, others covered in NURS 305)
5. Digoxin
▪increase contractility (positive inotrope)
▪decrease rate (negative chronotrope)
▪narrow therapeutic range (1-2 ng/dl)
▪toxicity (anorexia, n&v, arrhythmia)
▪Hypokalemia is a common cause of toxicity
▪loading dose
▪check apical pulse for one minute
▪ (hold for pulse < 60 )
6. Morphine Sulfate- decreases anxiety ( SNS), vasodilates decreasing afterload and the workload of the heart.
(other meds such as Entresto, Hydralazine etc covered in 305)
Nutritional considerations
▪sodium restricted
▪DASH diet from AHA
Less than 2 grams per day
▪Nursing considerations of HF
▪Health promotion
▪acute intervention * let’s link to treatment! Write interventions on the slide if you want to from inpatient
CHF Treatment Pathways:
▪__________________ intravascular volume
▪decrease venous return
▪improve __________ exchange
▪improve cardiac function
▪reduce anxiety
▪Chronic management
▪diet and weight
▪_________ therapy
▪rest
Hypertension
Definition: persistent elevation of
systolic BP ≥130-139 ( Stage 1)
140 or > (stage 2)
diastolic ≥ than 80-89 ( stage 1)
90 or greater Stage 2
*ACC/AHA/AAPA
▪Hypertension classifications
▪Essential HTN– (aka primary or idiopathic)
accounts for 90-95 % of all HTN
▪increased sympathetic nervous system stimulation
▪overproduction of sodium retaining hormones and vasoconstrictors
▪increased sodium intake
▪greater than ideal body weight
▪DM
▪ excessive alcohol intake
▪stress
Secondary HTN
accounts for 5-10% of all HTN
Treat underlying cause:
▪coarctation of the aorta (congenital narrowing)
▪renal disease (i.e. renal artery stenosis)
▪endocrine disorders (pheochromocytoma)
▪meds such as oral contraceptives and NSAIDS
▪-cocaine use
Categories of Hypertension
▪Clinical manifestations of HTN – often asymptomatic- silent
▪headache
▪easily fatigued
▪dizziness
▪blurred vision
▪epistaxis
▪Complications of HTN
▪CAD
▪CHF
▪cerebral vascular disease
▪nephrosclerosis
▪retinal damage
▪Diagnostics of HTN
▪BP measurements in both arms, 2 measurements 5 minutes apart
▪Labs : BUN, creatinine, urinalysis electrolytes, glucose
▪Chest x-ray and ECG
- Hypertension is not diagnosed on a single office visit. Come back for checks- 3 visits confirm the diagnosis.
▪Management of HTN
▪regular exercise
▪stress reduction
▪no smoking
▪medications in a stepwise approach
▪nutrition
▪Drug Therapy for HTN
PLEASE REVIEW AND KNOW
med chart p.687-689
Drug therapy for HTN
quick recap
1. Diuretics ( Thiazide, “diur”s) first line. Decrease preload/ intravascular volume. Watch potassium levels,
unless using K- sparing diuretics.
2. Beta Blockers (-‘lols) block beta receptors. Decrease HR and cardiac output, reduce sympathetic
vasoconstrictive tone. Watch HR, use cardioselective (beta 1)as indicated.
3. Calcium Channel Blockers (Cardizem, Verapamil and the ‘-pines) Vasodilate, decrease HR & contractility.
Monitor HR.
4. ACE Inhibitors (-prils) block conversion of angiotensin I to angiotensin II, prevent RAAS mediated
vasoconstriction. Watch for dry, hacking cough,
( Other classes…alpha blockers, direct vasodilators, ARBs etc.. Covered in Nurs 305)
▪Nutritional management HTN
▪Sodium restriction (2 GM per day)
▪caloric restriction
▪lower fats
Social
▪Smoking cessation
▪modify alcohol consumption
▪Stepwise plan of meds
Step 1 - non-pharmacological
Step 2 - thiazide diuretic, beta blocker, calcium channel blocker, or ACE inhibitor
Step 3 - add a second drug of a different class, increase 1st drug dose, or substitute
Step 4 - add a third drug or substitute
Step 5 - further evaluate, refer, or add a third or fourth drug
▪Inflammatory and Valvular heart disease- Self Study
A. Infective endocarditis
▪infection of the endocardial valve surface with microorganisms (usually bacterial)
▪occurs when turbulence within the heart allows organisms to infect (i.e. strep infection moves to
valves)
▪nonspecific clinical findings
▪treat with antibiotics
▪prophylactic antibiotics – use before surgery or dental procedures.
B. Acute pericarditis
▪inflammation of the pericardial sac
▪may be infectious cause, uremia, acute MI
▪symptoms include pleuritic rub, SOB, pericardial friction rub
▪pericardial effusion or tamponade complications
C. Mitral stenosis
▪most result from rheumatic fever
▪obstruction of flow out of left atrium
▪SOB, fatigue, palpitations, loud first heart sound, low pitched diastolic murmur
D. Mitral regurgitation
backflow of blood to L atrium from L ventricle
▪ex. Is mitral prolapse
▪asymptomatic for years
E. Aortic stenosis - age, rheumatic fever, CAD, calcification
F. Aortic regurgitation
- Leaf abnormality (i.e. 2 leafs present instead of 3)
- Endocarditis
Prosthetic valves
▪Mechanical (see illustration) pt. on anticoagulant for life
▪but more durable than bio valves
▪Biological (from pigs-porcine or cows- bovine) or homograft ( (human valve)
▪Vascular Disorders
Chronic arterial occlusive disease
Aortoiliac Disease (Leriche’s syndrome)
▪definition
▪pain in hip, buttocks or thighs
▪intermittent claudication
▪pulses absent or diminished in lower extremities
▪Surgery (aortofemoral graft)
Lower extremity disease (PAD)
▪progressive narrowing
▪femoral, popliteal, tibial, or peritoneal vessels
▪occurs in 60s or 80s
▪leading cause is atherosclerosis
▪smoking, HTN, hyperlipidemia, family history, DM, obesity, sedentary lifestyle
▪pain as disease progresses
▪Diagnosis of vascular disease
▪doppler ultrasound
▪duplex imaging – like an arteriogram (ultrasound of the vessels)
▪Management of vascular disease
▪Protect the extremity
▪slowing progression
▪decreasing vasospasm
▪improving collateral circulation
▪Surgery- endarterectomy, graft angioplasty, vascular bypass surgery.
▪Thrombophlebitis
▪Formation of a clot in association with inflammation of the vein
▪classified as superficial or deep
▪Virchow's Triad (high risk for DVT)
1-venous stasis (i.e. immobile patient)
2-damage to the endothelium ( HTN, chemicals,
hyperlipidemia, smoking etc.)
3-hypercoagulability (such as oral contraceptives, or
other coagulopathy)
▪Cardiovascular II
▪Dr. Mary Lynn Clarke
▪Associate Professor
▪Liberty University School of Nursing
▪Acute Coronary Syndrome
▪Management of Acute Coronary Syndrome THROMBINS2
▪Thienopyridines
▪Heparin/enoxaparin
▪Renin–angiotensin system blockers
▪Oxygen
▪Morphine
▪Beta blocker
▪Intervention
▪Nitroglycerin
▪Statin/salicylate
▪ED with Chest Pain
(Rule out MI)
Treatment (Use Acronym – MONA)
M- _________________*
O- _________________*
N- _________________
A- _________________
EKG
Cardiac enzymes
Diagnostic Cath Lab/ Interventional Cath
▪Angina
Progressive Disease
O2 demand > O2 supply → Myocardial Ischemia
Angina = Reversible Ischemia
Occurs when arteries are blocked 75% or more
Hypoxic within 10 seconds of occlusion
Viable for 20 minutes, then we see necrosis (MI)
Myocardial Infarction
_________________become irreversible and necrosis/ _______________ results.
Cardiac cells can withstand ischemia for approximately 20 min before death.
Earliest tissue to become ischemic is the sub-endocardium (_____________ layer).
Takes 4-6 hours for entire thickness of heart muscle to become necrotic.
______ of all MI’s are thrombus related.
▪Acute Myocardial Infarction – STEMI vs Non-STEMI
__________ - diseased vessel totally occluded by thrombus
_______ - diseased vessel partially occluded by thrombus
▪Clinical Manifestations of MI
Lack of oxygen and glucose leads to anaerobic metabolism
Lactic acid irritates nerve fibers → ________ in cardiac nerves
___________________ from transmission to the upper thoracic posterior nerve roots
▪Clinical Manifestations of MI
▪Pain
▪Nausea and Vomiting
▪Sympathetic stimulation
▪Fever
▪Cardiovascular dysfunction
▪Clinical Manifestations of MI
▪__________________ will stop in the area of cardiac cellular death
▪Degree of altered function depends on _______and______________________
▪most MI’s involve Lt. ventricle)
▪Infarctions described by area which correlates with the circulation (anterior, inferior, lateral,
septal, posterior etc.…)
▪Working to reverse occlusion and REPERFUSE and restore 02 to the tissues A.S.A.P.
▪Clinical Manifestations of MI - Healing
▪___________________________________ within ____ hours & enzymes are leaked from the
dead cardiac cells.
▪Proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by ___ days
→ thin wall. collagen matrix laid down.
▪Collateral circulation develops around infarcted area
▪_______________days post-MI - scar tissue is still weak -- myocardium especially vulnerable to
stress
▪_____________ - scar tissue is said to be healed
▪Scarred area:
Muscle is less compliant/uncoordinated wall motion
Ventricular dysfunction and/or
Pump failure can result
▪ Complications of MI
Dysrhythmias –very common
HF – damage causes permanent pump failure
Pericarditis- inflammation of the 2 layered sac can lead to cardiac tamponade.
Other serious complications: Cardiogenic shock
Papillary muscle rupture, ventricular aneurysm
(covered in NURS 460)
▪Diagnosis of MI
12-lead ECG
Enzymes
Troponin I
C reactive protein
CK-MB (CK2)
Cath Lab- coronary angiography to identify blockage
Management of MI
ICU/CCU
▪VS/ assessment/ cardiac monitor
▪Bedrest
▪arterial catheter – continuous BP readings
After……….. cardiac cath lab for
“REPERFUSION Therapy “ to restore 02 supply!
( _____________or ______________ Therapy)
▪Emergent PCI
▪Cath lab with Coronary angiography to visualize blockage
▪Balloon angioplasty- catheter with balloon tip, thread past blockage, inflate and compress plaque/blockage
against the vessel wall, see reperfusion with blood and 02 now passing through. ( Fig 33.6 and 33.7)
▪Stent – sits in vessel and acts as a straw or patent venue for blood flow and 02 delivery.
▪Patients have antiplatelet therapy post-stent
( page 714)
▪Coronary angiography
( A:identify blockage B: place stent)
▪Management of MI cont.
▪Fibrinolytic Therapy (“clot busting” )
▪rPA tPA ( recombinant tissue plasminogen activator) Only administered IV.
▪Contraindications ( see 33-15 p 724)
▪ active internal bleeding
▪History of intracranial hemorrhage
▪Intracranial or intraspinal surgery, recent
▪Recent ischemic stroke ( within past 3 mos.)
▪Severe, uncontrolled hypertension
▪Significant closed head injury or facial trauma
▪Suspected aortic dissection
▪No prior treatment with streptokinase within past 6 months
*IV Heparin drips also used alongside to prevent reocculsion
▪CABG- Coronary Artery Bypass Grafting
(coronary surgical revascularization)
▪What is it?
1. _________________________ of ________________ for blood transport between ___________ and
_________________________
2. allows for blood flow _____________beyond the stenosis
3. an artery is stenotic if its diameter is narrowed by more than
_________________________
4. Requires sternotomy and use of
cardiopulmonary bypass (CPB) machine.
▪CABG graft illustration
▪This illustration shows a heart with a saphenous vein graft. The surgeon connects the vein to the aorta
(upper left) and to the coronary artery at the (lower right)
▪How is it done?
__________ from the saphenous vein
▪vessel is _________________
▪anastomosed (attached/sewn)__________
to aorta and distally to the blockage.
▪Re-occlusion can occur
▪venous graphs tend to develop _______________
▪life expectancy of a venous graph- not as durable as arteries
▪ASA and statin therapy
▪Internal Mammary Artery (IMA)
▪Left IMA is ____________________to its point of origin from the left subclavian artery,
__________________ from chest wall and ___________________ to the coronary artery to the
stenosis
▪Right ______ can be used in a similar way
▪patency rate is ____________at 10 yr post procedure
▪Repeat CABG (gastroepiploic artery or epigstric artery)
▪Requires a ______________________ and _____________
▪wound complications ________________
▪other arteries tend to be more delicate
▪morbidity and mortality
▪nursing care: ____large surgical sites, assess for cardiac distress thru pain, arrhythmias, and complications
such as_______or drop in blood pressure, urinary output, change in pulses
▪MID-CABG OP-CABG
▪MID CABG
▪Minimally Invasive Direct -coronary artery bypass graft
▪uses a thoracotomy approach to mobilize the LIMA or the RIMA using beta blockers
▪before closure, meds are stopped
▪shorter recovery period
▪Visualization is not as good as open approach with obesity interfering.
▪OFF PUMP CABG
▪Open heart surgery without use of the CPBM
▪The surgeon is working on a eating heart using mechanical stabilizers.
▪Cardiopulmonary Bypass Machine
▪machine receives blood from the catheters in the vena cava or right atrium, oxygenates and returns via
pump to aorta
▪Management of cardiopulmonary bypass
1. Allows work on a ______________
2. machine pumps oxygenated blood
3. machine receives blood from the catheters in the vena cava or right atrium, _______________________ and
returns it via pump to aorta to perfuse the organs .
4. hypothermia is created
5. the longer the machine time, higher the chance of complications
▪Management of a CABG
▪Pre-op IV, antibiotics
▪procedures – general anesthesia, beta blockers, crack chest, CPB, grafting , closure,
sternal drains placed
▪post op complications:
▪hypovolemia --MI or CVA
▪cardiac tamponade -- wound infection
▪arrhythmia -- hemorrhage
▪emboli
▪fever
▪Nursing management of MI patients
▪Acute care
▪ cardiac monitor -- rest / comfort/02
▪pain control -- anxiety control
▪Chronic care
▪ cardiac rehabilitation
▪Risk of post- op depression
(see patient education in text
▪resumption of sexual activity, exercise, etc.)
▪ Drug Therapy
Chronic Stable Angina and ACS ( T.33-12 p 713)
ACE I’s- block conversion of angiotensin I to II
Antiplatelet aggregates- ASA, Plavix
Nitrates ( nitroglycerin) dilate coronary and peripheral vessels ↓ afterload, and ↓preload
Beta Blockers- block beta receptors, decrease heart rate, lower↓ workload of heart
Calcium Channel Blockers- decrease heart rate act as vasodilators ↓heart’s workload
Opioids-Morphine Sulfate, vasodilate/pain relief
(see other classes as well-
Anticoagulants ARBs, Thrombolytics, etc)
.
▪HF
Heart Failure
Definition
A cardiovascular state in which the____________is __________________ an adequate amount of blood to meet the
metabolic needs of the tissues. Not a disease but a condition.
The heart is a ________________pump.
According to American Heart Association
(AHA) there are about 6.5 million Americans with HF projections for a 46% rise in cases by the year 2030.
HF- The most common cause of hospitalizations in patients over the age of 65.
▪Risk Factors for HF
HTN/Hypertensive crisis
CAD/MI
Heart disease ( like Rheumatic fever, valve disorders, septal defects
Other see in textbook
Social:
DM
Smoking
Obesity, sedentary lifestyle
▪HF with reduced EF ( systolic)
vs HF with preserved EF ( diastolic)
Mixed HF- means you have both happening.
.
HFrEF/ Systolic Failure
The heart is a failing pump
Contractility is lost
Left ventricular EF ( ejection fraction) is lowered. Preload is backing up systemically. Less stroke volume SV) less
cardiac output (CO)
Normal EF- 55%- 65% volume is ejected with each beat. The remainder is healthy preload.
This number is lowered in Systolic Failure ( < 40% EF)
▪HFpEF/ Diastolic Failure
▪The ventricles are stiff/ cannot relax and fill during diastole.
▪Preserved EF means it ‘s normal, however, high filling pressures mean less stroke volume ( SV) less
cardiac output (CO).
IMPORTANT DIAGNOSTICS TO INCLUDE ON ALL HF PATHOS:
Echo – shows EF %, SV, CO
BNP – diagnostic lab >100 pg/mL
▪Left-Sided HF
▪Patho of left sided failure
▪blood backs up through the atrium to the _______
▪increased pressure causes fluid to leak out of the vessels = ___________congestion and impaired
exchange.
▪most common causes: CAD, HTN
Clinical manifestations incl :
Increased HR, crackles, s3 s4, pleural effusion,
altered mental status, restless/confused, weakness
Dyspnea, PND, frothy pink tinged sputum.
▪Patho of Right Sided HF
▪Weakened ventricle
▪primary cause is left sided failure,
▪Clinical Manifestations: Increased HR,
JVD, ascites, anasarca, hepatomegaly, splenomegaly, dependent edema, anorexia and GI bloating
▪Pitting Edema
▪Memorize this!!
Left sided HF “__________________”(back up into lungs)
Right sided HF “ _______________”(back up into systemically)
Cor Pulmonale = right sided failure comes
from COPD – chronic lung diseases or acutely from pulmonary embolism.
▪Compensatory mechanism for HF
1.Sympathetic nervous system
2.Dilation
3. renal response (RAAS)
4. Release of BNP, ANP
These all fail to help, because they work on the premise that we have a working pump. Because the heart has failed
as a pump, these worsen the problem, not help it!
▪Complications of HF
1. – refers to acute, life threatening condition- lung alveoli fill with fluid which increases
pulmonary pressures.
▪agitated, pale
▪cyanotic
▪severe dyspnea
▪wheezing, coughing, frothy, blood-tinged sputum
▪crackles
▪2. Pleural effusion
▪3. Left ventricle thrombus
▪4. hepatomegaly
▪5. Renal failure
▪Diagnostic factors for HF
1. exam
2. chest x-ray
3 12 lead _____________
4 . Hemodynamics (stroke volume, CO)
5 ECHO (looking at left ventricular ejection fraction) also cardiac cath, nuclear imaging
6. BNP (greater than _________ pg/mL), acute exacerbation.
▪Management of HF
▪Treat underlying cause
▪oxygen therapy and rest
▪Daily weights
▪Sodium restricted diet
▪Pharmacology
▪See table 34-7
▪Pharmacology for HF
▪1. Diuretics (i.e. Lasix)
▪Reduce _______ mobilize fluids
▪loop diuretics watch→ K levels
▪2. (ACE I)
▪ Reduce ____________
▪(i.e. Capoten, Vasotec, Lotensin)
3. Beta Blockers ( low dose)*
I.e. Coreg 3.25 mg po
4. (Digoxin)
▪Positive inotrope (↑contractility)
▪Negative chronotrope (↓ HR)
(Entresto, Hydralazine, others covered in NURS 305)
5. Digoxin
▪increase contractility (positive inotrope)
▪decrease rate (negative chronotrope)
▪narrow therapeutic range (1-2 ng/dl)
▪toxicity (anorexia, n&v, arrhythmia)
▪Hypokalemia is a common cause of toxicity
▪loading dose
▪check apical pulse for one minute
▪ (hold for pulse < 60 )
6. Morphine Sulfate- decreases anxiety ( SNS), vasodilates decreasing afterload and the workload of the heart.
(other meds such as Entresto, Hydralazine etc covered in 305)
▪Nutritional considerations
▪sodium restricted
▪DASH diet from AHA
Less than 2 grams per day
▪Nursing considerations of HF
▪Health promotion
▪acute intervention * let’s link to treatment! Write interventions on the slide if you want to from inpatient
CHF Treatment Pathways:
▪__________________ intravascular volume
▪decrease venous return
▪improve __________ exchange
▪improve cardiac function
▪reduce anxiety
▪Chronic management
▪diet and weight
▪_________ therapy
▪rest
▪Hypertension
Definition: persistent elevation of
systolic BP ≥130-139 ( Stage 1)
140 or > (stage 2)
diastolic ≥ than 80-89 ( stage 1)
90 or greater Stage 2
*ACC/AHA/AAPA
▪Hypertension classifications
▪Essential HTN– (aka primary or idiopathic)
accounts for 90-95 % of all HTN
▪increased sympathetic nervous system stimulation
▪overproduction of sodium retaining hormones and vasoconstrictors
▪increased sodium intake
▪greater than ideal body weight
▪DM
▪ excessive alcohol intake
▪stress
▪Secondary HTN
accounts for 5-10% of all HTN
Treat underlying cause:
▪coarctation of the aorta (congenital narrowing)
▪renal disease (i.e. renal artery stenosis)
▪endocrine disorders (pheochromocytoma)
▪meds such as oral contraceptives and NSAIDS
▪-cocaine use
▪Categories of Hypertension
▪Clinical manifestations of HTN – often asymptomatic- silent
▪headache
▪easily fatigued
▪dizziness
▪blurred vision
▪epistaxis
▪Complications of HTN
▪CAD
▪CHF
▪cerebral vascular disease
▪nephrosclerosis
▪retinal damage
▪Diagnostics of HTN
▪BP measurements in both arms, 2 measurements 5 minutes apart
▪Labs : BUN, creatinine, urinalysis electrolytes, glucose
▪Chest x-ray and ECG
- Hypertension is not diagnosed on a single office visit. Come back for checks- 3 visits confirm the diagnosis.
▪Management of HTN
▪regular exercise
▪stress reduction
▪no smoking
▪medications in a stepwise approach
▪nutrition
▪Drug Therapy for HTN
PLEASE REVIEW AND KNOW
med chart p.687-689
▪Drug therapy for HTN
quick recap
1. Diuretics ( Thiazide, “diur”s) first line. Decrease preload/ intravascular volume. Watch potassium levels,
unless using K- sparing diuretics.
2. Beta Blockers (-‘lols) block beta receptors. Decrease HR and cardiac output, reduce sympathetic
vasoconstrictive tone. Watch HR, use cardioselective (beta 1)as indicated.
3. Calcium Channel Blockers (Cardizem, Verapamil and the ‘-pines) Vasodilate, decrease HR & contractility.
Monitor HR.
4. ACE Inhibitors (-prils) block conversion of angiotensin I to angiotensin II, prevent RAAS mediated
vasoconstriction. Watch for dry, hacking cough,
( Other classes…alpha blockers, direct vasodilators, ARBs etc.. Covered in Nurs 305)
▪Nutritional management HTN
▪Sodium restriction (2 GM per day)
▪caloric restriction
▪lower fats
Social
▪Smoking cessation
▪modify alcohol consumption
▪Stepwise plan of meds
Step 1 - non-pharmacological
Step 2 - thiazide diuretic, beta blocker, calcium channel blocker, or ACE inhibitor
Step 3 - add a second drug of a different class, increase 1st drug dose, or substitute
Step 4 - add a third drug or substitute
Step 5 - further evaluate, refer, or add a third or fourth drug
▪Inflammatory and Valvular heart disease- Self Study
A. Infective endocarditis
▪infection of the endocardial valve surface with microorganisms (usually bacterial)
▪occurs when turbulence within the heart allows organisms to infect (i.e. strep infection moves to
valves)
▪nonspecific clinical findings
▪treat with antibiotics
▪prophylactic antibiotics – use before surgery or dental procedures.
B. Acute pericarditis
▪inflammation of the pericardial sac
▪may be infectious cause, uremia, acute MI
▪symptoms include pleuritic rub, SOB, pericardial friction rub
▪pericardial effusion or tamponade complications
C. Mitral stenosis
▪most result from rheumatic fever
▪obstruction of flow out of left atrium
▪SOB, fatigue, palpitations, loud first heart sound, low pitched diastolic murmur
D. Mitral regurgitation
backflow of blood to L atrium from L ventricle
▪ex. Is mitral prolapse
▪asymptomatic for years
E. Aortic stenosis - age, rheumatic fever, CAD, calcification
F. Aortic regurgitation
- Leaf abnormality (i.e. 2 leafs present instead of 3)
- Endocarditis
Prosthetic valves
▪Mechanical (see illustration) pt. on anticoagulant for life
▪but more durable than bio valves
▪Biological (from pigs-porcine or cows- bovine) or homograft ( (human valve)
▪Vascular Disorders
Chronic arterial occlusive disease
Aortoiliac Disease (Leriche’s syndrome)
▪definition
▪pain in hip, buttocks or thighs
▪intermittent claudication
▪pulses absent or diminished in lower extremities
▪Surgery (aortofemoral graft)
Lower extremity disease (PAD)
▪progressive narrowing
▪femoral, popliteal, tibial, or peritoneal vessels
▪occurs in 60s or 80s
▪leading cause is atherosclerosis
▪smoking, HTN, hyperlipidemia, family history, DM, obesity, sedentary lifestyle
▪pain as disease progresses
▪Diagnosis of vascular disease
▪doppler ultrasound
▪duplex imaging – like an arteriogram (ultrasound of the vessels)
▪Management of vascular disease
▪Protect the extremity
▪slowing progression
▪decreasing vasospasm
▪improving collateral circulation
▪Surgery- endarterectomy, graft angioplasty, vascular bypass surgery.
▪Thrombophlebitis
▪Formation of a clot in association with inflammation of the vein
▪classified as superficial or deep
▪Virchow's Triad (high risk for DVT)
1-venous stasis (i.e. immobile patient)
2-damage to the endothelium ( HTN, chemicals,
hyperlipidemia, smoking etc.)
3-hypercoagulability (such as oral contraceptives, or
other coagulopathy)
▪Clinical manifestations of thrombophlebitis
▪Superficial - palpable, firm cordlike vein which is tender, red and warm; may have fever and leukocytosis
▪Deep - may have no symptoms or have unilateral leg edema, pain, warm skin, and a temperature greater
than 38 Celsius
▪pain on flexion of foot (Homan’s sign) is classic but unreliable
▪DVT prophylaxis for immobilized pts in the hospital
( i.e. TEDS, foot pumps, DVT sleeves, Heparin or Lovenox subq.)
▪Complications of Thrombophlebitis
▪Pulmonary embolus
▪chronic venous insufficiency
▪Treatment of thrombophlebitis
▪Bedrest
▪elevation of extremity
▪warm, moist heat to relieve pain
▪anticoagulation therapy
▪surgery (rare)- use of a Greenfield filter is inserted (IVC filter).
Clinical manifestations of thrombophlebitis
▪Superficial - palpable, firm cordlike vein which is tender, red and warm; may have fever and leukocytosis
▪Deep - may have no symptoms or have unilateral leg edema, pain, warm skin, and a temperature greater
than 38 Celsius
▪pain on flexion of foot (Homan’s sign) is classic but unreliable
▪DVT prophylaxis for immobilized pts in the hospital
( i.e. TEDS, foot pumps, DVT sleeves, Heparin or Lovenox subq.)
▪Complications of Thrombophlebitis
▪Pulmonary embolus
▪chronic venous insufficiency
▪Treatment of thrombophlebitis
▪Bedrest
▪elevation of extremity
▪warm, moist heat to relieve pain
▪anticoagulation therapy
▪surgery (rare)- use of a Greenfield filter is inserted (IVC filter).
