lOMoARcPSD| 62788957
Patho/MedSurg II: Exam 2
Unit 5: Cardiac Alterations in Cardiac Function
CH:18, 19
Book & PPT, MEDSURG, KEY POINTS, Lecture
Chapter 18
Coronary Heart Disease
• Coronary heart disease (CHD): also called ischemic heart disease and coronary artery disease (CAD)
• Endothelial cell dysfunction: inner lining of small arteries that don’t function normally a:ects tissues
• Characterized by insuUcient delivery of oxygenated blood to the myocardium caused by
atherosclerotic coronary arteries (CAD) Sequelae of CHD includes:
o Angina pectoris: chest pain, decreased blood Aow to the heart, discomfort from CHD
o Myocardial infarction: blockage of blood Aow to the heart muscle (heart attack)
o Dysrhythmias: CHD can weaken heart muscle and lead to HF and dysrhythmias
o Heart failure
o Sudden cardiac death: 50% of all deaths are from CVD. Can occur initially or right after an MI
• Risk Factors
o NonmodiXable Risks
Age: ≥45 years for men; ≥55 years for women
Gender: male (earlier onset, usually by 10 yrs.)
Family history of premature coronary heart disease
Myocardial infarction (MI) or sudden cardiac death in
• male Srst-degree relative at age less than 55 years or
• female Srst-degree relative at age less than 65 years
Genetic markers identiSed o Atherosclerosis is the source of nearly all CHD. It causes
progressive narrowing of the arterial lumen
• Dx o Signs and symptoms
o EKG tells us any abnormalities in heart rhythm a:ecting the heart now, or prior damage
o Heart Cath catheter in an artery of the groin or arm that gets threaded to the heart in order
to visualize blockages or damage
• CM o Chest pain o Fatigue, weakness o Heavy chest pressure o N/V, dyspnea
o Prolonged or severe ischemia = cardiac arrest
Angina***
• Chest pain Angina Pectoris o associated with intermittent myocardial ischemia.
• KEY POINT: characterized by intermittent bouts of chest pain triggered by exertion and generally
relieved by rest. No permanent myocardial damage occurs.
o ECG changes include ST-segment elevation (or depression), large Q waves, and inverted T
waves.
• Etiology
• Patho
• CM o Pain may be described as Burning, crushing, squeezing, choking o Elephant sitting on chest o
Mistaken for indigestion, dental pain o Chest pain
o Pain radiates to neck, jaw, shoulders, upper left arm
• May result in ine_cient cardiac pumping with resultant pulmonary congestion and shortness of breath
• Three patterns o Stable or typical angina
Most common; Also called classic
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Characterized by stenotic atherosclerotic coronary vessels
Onset of anginal pain is generally predictable and elicited by similar stimuli each time
Relieved by rest and nitroglycerin *** causes coronary and peripheral vasodilation,
reduces preload, and reduces myocardial workload.
Unstable angina may progress acute ischemia
Caused by: atherosclerosis, intermittent myocardial ischemia, Sympathetic nervous
system, increased preload/afterload/HR
Induced by exercise, cold, stress
Predictable & Elicited by similar stimuli each time (pain) o Prinzmetal or variant
angina
D: Unpredictable attacks of anginal pain
Onset of symptoms is unrelated to physical or emotional exertion, heart rate, or other
obvious causes of increased myocardial oxygen demand.
Characterized by
• vasospasms
• atherosclerosis-induced hypercontractility,
• abnormal secretion of vasospastic chemicals by local mast cells
• abnormal calcium Aux across vascular smooth muscle
Responds well to treatment with calcium channel–blocking drugs o Unstable angina (or
crescendo) May progress to acute ischemia
D: ACS Acute Coronary Syndrome: chest pain that may be more severe and last longer
than typical angina
Plaque rupture with subsequent acute thrombus development is thought to occur.
The occlusion is partial, or the clot is dissolved before the death of myocardial tissue
Unpredictable, Occurs at rest, Confused w/ MI
ST Segment elevation
• All patients with angina are at risk for developing ACS and need aggressive treatment for risk
reduction. o Risk factor: plaque rupture, thrombus, and dysrhythmia
MEDSURG
o Dx
Patient hx,
ECG
Cardiac biomarkers: Troponin, CPK
Stress test/ Nuclear scan
Invasive procedure (cardiac cath or coronary angiograph) o Medical Care
Beta-Blockers (Atenolol, Metoprolol)
Calcium Channel Blockers (Diltiazem, Nifedipine)
Anticoagulant (Heparin, Lovenox)
MONA (morphine, oxygen, nitroglycerin, and aspirin) o Nursing Care
Control risk factors
Reduce o2 demands
O2
MONA (morphine, Oxygen, Nitroglycerine, and aspirin)
Assess patient, Vital signs
Response to medication o NI
Priority
Patient is to stop all activity and sit or rest in bed (semi-Fowler positioning)
Assess the patient while doing interventions.
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• Assessment includes VS, observation for respiratory distress, pain. In the
hospital ECG is assessed or obtained
Administer medication NTG. Reassess pain and administer NTG up to three doses
• What is the typical protocol?
Administer oxygen 2 L/min by nasal cannula Patient teaching:
Myocardial Infarction***
• MI results when prolonged or total disruption of blood Aow to the myocardium causes cellular death
by necrosis or apoptosis.
o Damage to the heart muscle = no blood supply
• Etiology o Thrombus/Atherosclerosis a thrombus on top of an ulcerated or cracked atherosclerotic
plaque. Change in structure of plaque
• Patho o No blood `ow, death to tissues, distal to blockage CM
o Severe, crushing, excruciating chest pain radiate to the arm, shoulder, jaw, or back is the
harbinger of MI. usually on left side
o Pain accompanied by nausea, vomiting, diaphoresis (sweating), and shortness of breath
either on exertion or at rest
o Discomfort in chest region o Pressure and tightness in chest
Valvular Diseases
Mitral Valve (Stenosis, Regurgitation, and Prolapse) ***
Stenosis***
• Narrowing of mitral valve
Etiology
• Damage from Rheumatic heart disease
• Calcium deposits around the vale
• Congenital defect of the mitral valve
• Radiation therapy
• Lupus
Patho
• Blood Aow from left atrium to left ventricle impaired during ventricular diastole
• Decreased stroke volume
• Can lead to enlargement of the Left atrium
• Back up of blood in the lungs and right side of the heart
CM Low-pitched rumble
• Atrial enlargement, decreased stroke volume (seen on echo)
• Dysrhythmias
• Dizzy, fatigue, dyspnea, chest pain,
• Pulmonary congestion
• Others are asymptomatic
• Symptoms exacerbated by decrease left ventricular Slling such as increased HR
• S/S of mitral stenosis secondary to pulmonary congestion may include orthopnea,
cough, dyspnea on exertion, paroxysmal nocturnal dyspnea, abnormal breath sounds,
and poor arterial oxygenation.
• Reduced left ventricular stroke volume = fatigue, poor activity tolerance, and
weakness.
Downloaded by NGINA MINA ()
Patho/MedSurg II: Exam 2
Unit 5: Cardiac Alterations in Cardiac Function
CH:18, 19
Book & PPT, MEDSURG, KEY POINTS, Lecture
Chapter 18
Coronary Heart Disease
• Coronary heart disease (CHD): also called ischemic heart disease and coronary artery disease (CAD)
• Endothelial cell dysfunction: inner lining of small arteries that don’t function normally a:ects tissues
• Characterized by insuUcient delivery of oxygenated blood to the myocardium caused by
atherosclerotic coronary arteries (CAD) Sequelae of CHD includes:
o Angina pectoris: chest pain, decreased blood Aow to the heart, discomfort from CHD
o Myocardial infarction: blockage of blood Aow to the heart muscle (heart attack)
o Dysrhythmias: CHD can weaken heart muscle and lead to HF and dysrhythmias
o Heart failure
o Sudden cardiac death: 50% of all deaths are from CVD. Can occur initially or right after an MI
• Risk Factors
o NonmodiXable Risks
Age: ≥45 years for men; ≥55 years for women
Gender: male (earlier onset, usually by 10 yrs.)
Family history of premature coronary heart disease
Myocardial infarction (MI) or sudden cardiac death in
• male Srst-degree relative at age less than 55 years or
• female Srst-degree relative at age less than 65 years
Genetic markers identiSed o Atherosclerosis is the source of nearly all CHD. It causes
progressive narrowing of the arterial lumen
• Dx o Signs and symptoms
o EKG tells us any abnormalities in heart rhythm a:ecting the heart now, or prior damage
o Heart Cath catheter in an artery of the groin or arm that gets threaded to the heart in order
to visualize blockages or damage
• CM o Chest pain o Fatigue, weakness o Heavy chest pressure o N/V, dyspnea
o Prolonged or severe ischemia = cardiac arrest
Angina***
• Chest pain Angina Pectoris o associated with intermittent myocardial ischemia.
• KEY POINT: characterized by intermittent bouts of chest pain triggered by exertion and generally
relieved by rest. No permanent myocardial damage occurs.
o ECG changes include ST-segment elevation (or depression), large Q waves, and inverted T
waves.
• Etiology
• Patho
• CM o Pain may be described as Burning, crushing, squeezing, choking o Elephant sitting on chest o
Mistaken for indigestion, dental pain o Chest pain
o Pain radiates to neck, jaw, shoulders, upper left arm
• May result in ine_cient cardiac pumping with resultant pulmonary congestion and shortness of breath
• Three patterns o Stable or typical angina
Most common; Also called classic
Downloaded by NGINA MINA ()
, lOMoARcPSD| 62788957
Characterized by stenotic atherosclerotic coronary vessels
Onset of anginal pain is generally predictable and elicited by similar stimuli each time
Relieved by rest and nitroglycerin *** causes coronary and peripheral vasodilation,
reduces preload, and reduces myocardial workload.
Unstable angina may progress acute ischemia
Caused by: atherosclerosis, intermittent myocardial ischemia, Sympathetic nervous
system, increased preload/afterload/HR
Induced by exercise, cold, stress
Predictable & Elicited by similar stimuli each time (pain) o Prinzmetal or variant
angina
D: Unpredictable attacks of anginal pain
Onset of symptoms is unrelated to physical or emotional exertion, heart rate, or other
obvious causes of increased myocardial oxygen demand.
Characterized by
• vasospasms
• atherosclerosis-induced hypercontractility,
• abnormal secretion of vasospastic chemicals by local mast cells
• abnormal calcium Aux across vascular smooth muscle
Responds well to treatment with calcium channel–blocking drugs o Unstable angina (or
crescendo) May progress to acute ischemia
D: ACS Acute Coronary Syndrome: chest pain that may be more severe and last longer
than typical angina
Plaque rupture with subsequent acute thrombus development is thought to occur.
The occlusion is partial, or the clot is dissolved before the death of myocardial tissue
Unpredictable, Occurs at rest, Confused w/ MI
ST Segment elevation
• All patients with angina are at risk for developing ACS and need aggressive treatment for risk
reduction. o Risk factor: plaque rupture, thrombus, and dysrhythmia
MEDSURG
o Dx
Patient hx,
ECG
Cardiac biomarkers: Troponin, CPK
Stress test/ Nuclear scan
Invasive procedure (cardiac cath or coronary angiograph) o Medical Care
Beta-Blockers (Atenolol, Metoprolol)
Calcium Channel Blockers (Diltiazem, Nifedipine)
Anticoagulant (Heparin, Lovenox)
MONA (morphine, oxygen, nitroglycerin, and aspirin) o Nursing Care
Control risk factors
Reduce o2 demands
O2
MONA (morphine, Oxygen, Nitroglycerine, and aspirin)
Assess patient, Vital signs
Response to medication o NI
Priority
Patient is to stop all activity and sit or rest in bed (semi-Fowler positioning)
Assess the patient while doing interventions.
Downloaded by NGINA MINA ()
, lOMoARcPSD| 62788957
• Assessment includes VS, observation for respiratory distress, pain. In the
hospital ECG is assessed or obtained
Administer medication NTG. Reassess pain and administer NTG up to three doses
• What is the typical protocol?
Administer oxygen 2 L/min by nasal cannula Patient teaching:
Myocardial Infarction***
• MI results when prolonged or total disruption of blood Aow to the myocardium causes cellular death
by necrosis or apoptosis.
o Damage to the heart muscle = no blood supply
• Etiology o Thrombus/Atherosclerosis a thrombus on top of an ulcerated or cracked atherosclerotic
plaque. Change in structure of plaque
• Patho o No blood `ow, death to tissues, distal to blockage CM
o Severe, crushing, excruciating chest pain radiate to the arm, shoulder, jaw, or back is the
harbinger of MI. usually on left side
o Pain accompanied by nausea, vomiting, diaphoresis (sweating), and shortness of breath
either on exertion or at rest
o Discomfort in chest region o Pressure and tightness in chest
Valvular Diseases
Mitral Valve (Stenosis, Regurgitation, and Prolapse) ***
Stenosis***
• Narrowing of mitral valve
Etiology
• Damage from Rheumatic heart disease
• Calcium deposits around the vale
• Congenital defect of the mitral valve
• Radiation therapy
• Lupus
Patho
• Blood Aow from left atrium to left ventricle impaired during ventricular diastole
• Decreased stroke volume
• Can lead to enlargement of the Left atrium
• Back up of blood in the lungs and right side of the heart
CM Low-pitched rumble
• Atrial enlargement, decreased stroke volume (seen on echo)
• Dysrhythmias
• Dizzy, fatigue, dyspnea, chest pain,
• Pulmonary congestion
• Others are asymptomatic
• Symptoms exacerbated by decrease left ventricular Slling such as increased HR
• S/S of mitral stenosis secondary to pulmonary congestion may include orthopnea,
cough, dyspnea on exertion, paroxysmal nocturnal dyspnea, abnormal breath sounds,
and poor arterial oxygenation.
• Reduced left ventricular stroke volume = fatigue, poor activity tolerance, and
weakness.
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