Week 7: Cardiovascular Disorders Flashcards
The Cardiovascular System
Consists of the: Blood, Heart, Blood vessels
-Carries nutrients & oxygen to cells throughout the body
-Increases blood flow to meet energy demands (i.e. physical activity)
-Stops bleeding & promotes healing (i.e. site of injury or bleeding)
-Produces & carries white blood cells & antibodies (defense)
-Regulates body temperature:
(Heat from muscles carried through body)
(Blood vessels dilate to cool body or constrict to conserve heat)
Heart- Great Vessels
Vena Cava
Pulmonary Arteries: to the lungs
Pulmonary Veins: to the heart
Aorta: pumps blood, oxygen, nutrients to where it needs to go
Heart- Pump
Heart –> double pump
-Pulmonary circulation: to the lungs
-Systemic circulation: to the body
Heart- 3 Layers
Endocardium
-Inner layer
-Continuous with vessels
Myocardium
-Middle layer
-Thick and muscular
-Cardiac muscle
Epicardium
-Outer layer
-Forms pericardium
Pericardium
-Sling like membrane
-Supports the heart by attaching it to other structures (diaphragm, large blood vessels)
Blood Flow Through the Heart
Deoxygenated Blood:
Right atrium
-Receives blood from body (vena cava)
Right Ventricle
* receives blood from right atrium
* pumps to lungs via pulmonary artery
Oxygenated Blood
Left Atrium
-Receives blood from lungs (pulmonary veins)
Left Ventricle
-Receives blood from left atrium
-Pumps to body via aorta
Cardiac Cycle: One Heartbeat
Systole (contraction) & diastole (relaxation) act in coordination
Cardiac Conduction System
Cardiac Impulse (action potential) spreads throughout the heart
-Specialized conduction tissue
Arises in the SA node (pacemaker of the heart)
and spreads over the atria
-SA node originates the cardiac impulse
-Atria contract
Goes to the AV node and spreads over the ventricles
-AV node slows cardiac impulse and sends it to bundle of His
-Bundle of His send the cardiac impulse to Purkinje fibers through the ventricles
-Ventricles contract
Cardiac Conduction System- ECG
Waves
P = atrial depolarization
QRS = depolarization of the ventricles
T = repolarization of the ventricles
U = repolarization of the purkinje fibres or might be hypokalemia
Cardiac Mechanical System
-Depolarization triggers mechanical activity
Systole
-Contraction of the myocardium
-Results in ejection of blood from the cardiac chamber
Diastole
-Relaxation of the myocardium
-Allows for filling of the chamber
Cardiac Output (CO)
-Measurement of the heart’s mechanical efficiency
-Amount of blood pumped by each ventricle in 1 minute
Stroke Volume (SV)= the amount of blood ejected from the ventricle with the heartbeat
Factors Affecting Cardiac Output (CO)
The HR is regulated primarily by the autonomic nervous system
Factors Affecting the SV:
-Preload
-Contractility
-Afterload
Increases in preload, contractility, and afterload (increases workload of the myocardium), results in increased oxygen demand
Cardiac Reserve
Ability of the heart to respond to stress by increasing CO as much as three-fold or four-fold. Can increase HR to 180 bpm for short periods without hard
Blood Vessels- Function
-Act as a delivery system
-Regulate blood pressure
-Exchange nutrients and waste between the capillaries and cells
-Redistribute blood in response to changes in body needs
-Helps regulate body temperature
Types of Blood Vessels
-Arteries: thick surrounding for pumping blood
(arterioles)
-Capillaries: thin surrounding for gas exchange
-Veins
(Venules)
Regulation- Autonomic Nervous System
Sympathetic (stress)
-Fight or flight
-SA node activity and heart rate
-Speed of cardiac impulse through conduction system
-Force of myocardial contraction
Parasympathetic (peace)
-SA node activity and heart rate
-Speed of cardiac impulse from SA to AV node
-No effect on strength of contraction
Blood Pressure
Arterial BP: measure of the pressure exerted by blood against the walls of the arterial system
Systolic BP: the peak pressure exerted against the arteries when the heart contracts
Diastolic BP: the residual pressure of the arterial system during ventricular relaxation
Age Related Considerations
-Age is the greatest risk factor for CV disease
-Most common cause of hospitalization and second leading cause of death in adults < 85
-Cardiac Valves: thicker and stiffer
-Decreased # pacemaker cells (dysrhythmias)
-Arterial and venous blood vessels thicken and become less elastic
-Valves in the veins in the lower extremities
(reduced ability to return blood to the heart)
(often results in dependent edema)
Assessment- Subjective Data
History:
-Chest pain
-SOB
-Hypertension
-Stroke
-Smoking
-Edema
Medications
-OTC
-Prescription
-ASA (aspirin)
-NSAIDs
-Blood Thinners
Surgery or other treatments
-related to CV problems
Assessment- Objective Data
Measures: general appearance, vital signs
Inspection: skin, extremities (edema, lesions) neck veins, capillary refill
Palpation: bilateral and carotid pulses 2+, (symmetry, quality, rhythm,) lower extremities (edema)
Auscultation: carotid and femoral arteries, abdominal aorta, heart (extra sounds, murmurs)
Assessment- Pulses
0: absent
1+: weak, thready
2+: normal
3+: full, bounding
Assessment: Cardiac Auscultation
-The movement of the cardiac valves creates some turbulence in the blood flow, the resulting heart sounds are normal
S1: closure of the tricuspid and mitral valves, soft “lubb” (beginning of systole)
S2: closure of the aortic and pulmonic valves, sharp “dupp” (beginning of diastole)
Invasive Diagnostics
Cardiac catheterization
Coronary angiography
Intravascular ultrasonography
Hemodynamic monitoring
Noninvasive Diagnostics
Chest x-ray
Electrocardiography
(Electrocardiogram (ECG))
(Stress testing)
(Echocardiography)
Nuclear cardiography
Cardiovascular MRI (CMRI)
Cardiac CT
Blood studies
Common Medications
Atenolol: hypertension
Nitroglycerin: angina
Furosemide: heart failure
Alteplase: myocardial infarction
Hypertension
-Persistent BP measurements above the normal systolic/diastolic pressures 120/80
-Must occur on 2 consecutive occasions
-Persistent systolic BP > 140 mmHg or
-Persistent diastolic BP > 90 mmHg
*Most significant modifiable risk factor for cardiovascular disease and mortality in Canada
-Responsible for up to 50% of deaths due to heart disease & stroke
~20% of Canadian adults have hypertension
Hypertension
Even small incremental changes in systolic and diastolic pressures have a direct effect on mortality:
-For every 20-mm Hg increase in systolic BP or a 10-mm Hg increase in diastolic BP, the risk for cardiovascular mortality doubles
As blood pressure increases, so does risk for:
-MI
-Heart failure
-Stroke
-Renal Disease
Subtype of Hypertension
Isolated Systolic Hypertension (ISH)
-Sustained elevation of SBP ≥ 140 mm Hg and a DBP < 90 mm Hg
-Common in older adults related to loss of elasticity in large arteries
Hypertension Classifications
Primary (essential) hypertension:
-Elevated BP without an identified cause
-Does not have a single known cause, but certain risk factors
-90% to 95% of clients
Secondary Hypertension
-Elevated BP with a specific cause
-5% to 10% in adults; >80% in children
-Many causes; treatment aimed at eliminating the underlying cause
Primary Hypertension Risk Factors
Advancing Age: 50% of people >65
Heavy alcohol use
Smoking > 15 cigarettes / day
Diabetes
Elevated serum lipids
High dietary sodium
Gender: < 55 (men) > 55 (women)
Family history
Obesity
Ethnicity: black and south asian
Sedentary Lifestyle
Socioeconomic Status: low income
Psychosocial stress
Secondary Hypertension- Causes
- Coarctation or congenital narrowing of the aorta
-Renal disease (renal artery stenosis and parenchymal disease)
-Endocrine disorders (cushing syndrome and hyperaldosteronism)
-Neurological disorders (brain tumours, quadriplegia, head injury)
-Pregnancy induced hypertension
-Sleep apnea
-Medications
Signs & Symptoms
None initially “silent killer”
Usually found during check-ups
Severe Hypertension: related effects on blood vessels or increase workload of the heart:
Fatigue, decreased activity tolerance, dizziness, palpitations, angina, dyspnea
Complications
The most common complications of hypertension are target-organ diseases occuring in the
HEART (hypertensive heart disease)
BRAIN (cerebrovascular disease)
PERIPHERAL VASCULATURE (PAD)
KIDNEYS (nephrosclerosis)
EYES (retinal damage)
-CAD related to atherosclerosis
-Left ventricular hypertrophy related to increased cardiac workload
-Heart failure related to inability to pump enough blood to meet demands
-Stroke related to atherosclerosis
-Intermittent claudication related to atherosclerosis
-Ischemia related to narrowed intrarenal blood vessels
-Blurring, vision loss
Hypertension- Diagnostics
-Blood pressure monitoring
-Urinalysis
-Blood chemistry
-Fasting blood glucose
-Fasting total cholesterol & high- density lipoprotein, low-density lipoprotein, and triglycerides
-Standard 12-lead electrocardiography
-Assess urinary albumin excretion in clients with diabetes
-All clients with treated hypertension need to be monitored for the appearance of diabetes
Hypertension Collaborative Care
Lifestyle Modifications
-Nutritional therapy: Dietary Approaches to Stop Hypertension (DASH) diet
-Decreased salt intake: most cost-effective measure to improve health outcomes
-Weight reduction
-Limit alcohol consumption
-Physical activity
-Avoidance of tobacco products – CV benefits seen within 1 year
-Stress management
Hypertension Collaborative Care
Drug therapy- goal is to achieve a BP of <140/90 mmHg
Current drugs have two main actions:
-To reduce SVR, and
-To decrease the volume of circulating blood
Drug Types:
-Diuretics
-Adrenergic (sympathetic) inhibitors
-Direct vasodilators
-Angiotensin inhibitors
-Calcium channel blockers
Nursing Management
Goals- the patient will:
-Achieve and maintain the determined target BP
-Understand, accept, & implement the therapeutic plan
-Experience minimal or no unpleasant adverse effects of therapy
-Be confident about the ability to manage & cope with this condition
Health Promotion:
-Dietary modifications
-Screening programs in the community
-Cardiovascular risk factor modification
Ambulatory & Home Care:
-Physical activity
-Home blood pressure monitoring
-Client adherence treatment
Age-Related Considerations
-Hypertension is common in 60+
-Loss of tissue elasticity
-Increased collagen content & stiffness of the myocardium
-Increased peripheral vascular resistance
-Decreased β- adrenergic receptor sensitivity
-Decreased kidney function
-Decreased renin response to sodium & water depletion
-Impaired baroreceptor reflex mechanisms-risk for orthostatic hypotension
Hypertensive Crisis
Severe, abrupt increase in DBP (defined as >120–130 mm Hg)
Rate of increase in BP is more important than the absolute value
Risk: history of hypertension and failure to comply with treatment
Hypertensive Emergency is evidence of acute target-organ damage
-Hypertensive encephalopathy, cerebral hemorrhage
-Acute renal failure
-Myocardial infarction
-Acute left ventricular failure with pulmonary edema
-Aortic aneurysm
Hypertensive Crisis (Nursing Collaborative Care)
BP level alone is a poor indicator of the seriousness of the patient’s condition and is not the major factor in deciding the treatment for
a hypertensive crisis
The association between elevated BP and signs of new or progressive end- organ damage determines the seriousness of the situation.
Nursing / Collaborative Care
-IV drug therapy: decrease mean arterial pressure
-Monitor cardiac & renal function
-Neurological checks
-Determines cause
-Education to avoid future crises
Atherosclerosis
Chronic Endothelial Injury
-Hypertension
-Tobacco use
-Hyperlipidemia
-Hyperhomocysteinemia
-Diabetes
-Infection
-Toxins
Fatty Streak
-Lipids accumulate and migrate into smooth muscle cells
Fibrous Plaque
-Collagens covers the fatty streak
-Vessel lumen is narrowed
-Blood flow is reduced
-Fissures can develop
Complicated Lesion
-Plaque rupture
-Thrombus formation
-Further narrowing or total occlusion of vessel
Acute Coronary Syndrome
-Associated with deterioration of an atherosclerotic plaque that was once stable
Unstable Angina (UA)
-Chest pain that is new in onset, occurs at rest, or has worsening pattern
-Unpredictable
-Emergency
-May become an NSTEMI
Myocardial Infarction (MI)
-Results from sustained ischemia, causing irreversible myocardial cell death –EMERGENCY
-80-90% occurs secondary to thrombus formation
-Contractile function of the heart stops in the necrotic areas
-STEMI & NSTEMI
MI- NSTEMI
Non-ST-segment elevation MI
Partial occlusion
Damage (partial thickness)
Pathological Q waves not usual
MI- STEMI
ST-segment elevation MI
Total occlusion
More extensive damage (full thickness)
Pathological Q-waves present
Pain Associated with the Heart
Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI
Atherosclerosis- Stents & Bypass
Percutaneous Coronary Intervention (PCI)
Coronary Artery Bypass graft (CABG)
Fibrinolytic Therapy
Aimed at stopping the infarction process by dissolving the thrombus in the coronary artery and reperfusing the myocardium
-Must be given as soon as possible
-Single IV bolus over 30-90 mins
-Major complication: bleeding
Rhythm Identification and Treatment
-The ability to recognize normal & abnormal cardiac rhythms is an essential nursing skill
-Prompt assessment of abnormal cardiac rhythms, called dysrhythmias, and of the patient’s response to them is critical
Cardiac Cells (Automaticity)
Ability to initiate an impulse spontaneously and continuously
Cardiac Cells (Contractility)
Ability to respond mechanically to an impulse
Cardiac Cells (Conductivity)
Ability to transmit an impulse along a membrane in an orderly manner
Cardiac Cells (Excitability)
Ability to be electrically stimulated
Electrocardiogram (ECG)
-Graphic tracing of electrical impulses produced by the heart
-Waveforms of ECG represent activity of charged ions across membranes of myocardial cells
-Typically, there are 12 recording leads in the ECG
-Six leads (leads I, II, III, aVR, aVL, & aVF) measure electrical forces in the frontal plane
-Six leads (V1–V6) measure electrical forces in the horizontal plane
ECG Monitoring
-The ECG can be visualized continuously on a monitor oscilloscope
-A recording of the ECG (rhythm strip) is obtained on ECG paper attached to the monitor
-The recording provides documentation of the patient’s rhythm
-It also allows for measurement of complexes and intervals, and for assessment of dysrhythmias
12-Lead ECG
-A lead is a glimpse of the electrical activity of the heart from a particular angle
(a lead is a perspective)
-There are 10 electrodes providing 12 perspectives of the heart’s activity using different angles through two electrical planes
(vertical and horizontal planes)
-When being continuously monitored, between 1 & 12 ECG leads may be used
Impulse Formation
-Disorders of impulse formation can cause dysrhythmias
-Normally, the main pacemaker of the heart is the SA node, which spontaneously
discharges 60-100x/min
-Secondary pacemakers may originate from the AV node (40 to 60x/min) or the His–Purkinje system (20 to 40x/min)
Sinus Bradycardia
-SA node fires at a rate <60 bpm
-May be normal in trained athletes
-Tx = atropine or pacemaker
Sinus Tachycardia
-SA node fires at a rate >100bpm
-Physiological and psychological stressors
-Tx = treat the underlying cause
Premature Atrial Contraction (PAC)
-Contraction originates in the atrium from a focus other than the SA node, travels in an abnormal way
-Stress, fatigue, substances and other medical conditions
-Tx = withdrawal of sources of stimulation
Paroxysmal Supraventricular Tachycardia (PSVT)
-Originates in a focus above the bundle of His
-Overexertion, emotional stress, and stimulants
-Tx = vagal stimulation (valsalva & coughing), IV adenosine
Atrial Flutter
-Atrial tachydysrhythmias: recurring, regular, sawtooth-shaped flutter
-Disease states: CAD, hypertension, cardiomyopathy, etc
-Tx = low ventricular response by calcium channel blockers and β- adrenergic blockers. Convert flutter by amiodarone, propafenone. May need cardioversion (shock)
Atrial Fibrillation (A-Fib)
-Total disorganization of atrial electrical activity leading to loss of effective atrial contraction
-Underlying heart disease (CAD, HF, pericarditis)
-Tx = decrease ventricular rate by CCB and beta-adrenergic blockers (metoprolol); or anticoagulation therapy
Junctional Dysrhythmias
-Originate in AV node because SA node failed to fire, AV node becomes pacemaker, safety mechanism when SA fails
-CAD, HP, inferior MI, electrolyte imbalances
-Tx = atropine, beta-adrenergic blockers, CCBs, and amiodarone
AV Block- 1st Degree
-Duration of AV conduction (PR interval) is prolonged
-MI, CAD, hyperthyroidism, vagal stimulation, some meds
-Tx = none; may need to adjust meds that are causing it
Premature Ventricular Contractions (PVCs)
-Contractions originating in the ventricles (wide distorted QRS)
-Stimulants (caffeine, nicotine), epinephrine, electrolyte imbalances, MI, HF, CAD
-Tx = based on the cause, O2, or may not be treated
Ventricular Tachycardia (V-tach)
-When a run of three or more PVCs occurs, ventricles take over as pacemaker
LIFE THREATENING
-MI, CAD, CNS disorders
-Tx = treat the precipitating cause
Ventricular Fibrillation (V-fib)
-Severe derangement of the heart rhythm: irregular undulations of varying shapes and amplitude on the ECG
-Mechanically, the ventricle is simply “quivering” and no effective contraction: no cardiac output occurs
-MI, myocardial ischemia, CAD
- Tx = assess airway, breathing, pulse
-CPR, Defibrillation
Asystole
-Total absence of ventricular electrical activity. On occasion, P waves are detected
-No ventricular contraction occurs because depolarization does not occur. Patients are unresponsive, pulseless, and apneic
Defibrillation
-Most effective method of terminating ventricular fibrillation and pulseless VT
-Accomplished by the passage of a DC electric shock through the heart that is sufficient to depolarize the cells of the myocardium
-The intent is that subsequent repolarization of myocardial cells allows the SA node to resume the role of pacemaker
-Upon defibrillation, the operator calls, “All clear” and looks to see that personnel are not touching the patient or the bed at the time of
defibrillator discharge
-It is essential that the operator ensures that all personnel are clear before the defibrillator is discharged
Artificial Cardiac Pacemakers
-Electronic device used to pace the heart when the normal conduction pathway is damaged or diseased
-The electrical signal (stimulus) travels from the pacemaker, through the leads, to the wall of the myocardium which then contracts
