Class 1 CV Flashcards
Premature VS (HR, BP, RR)
120-170HR
>55/35>75/45
40-70RR
0-3 month VS (HR, BP, RR)
100-160HR
>65/45>85/55
30-60RR
3-6 month VS (HR, BP, RR)
90-120HR
>70/50>90/65
30-45RR
6-12 month (HR, BP, RR)
80-120HR
>80/55>100/65
25-40 RR
1-3 year VS (HR, BP, RR)
70-110HR
>90/55>105/70
20-30RR
6-12 year VS (HR, BP, RR)
60-95HR
>100/60>120/75
14-22RR
12+ year VS (HR, BP, RR)
55-85HR
>110/65>135/85
12-18RR
Palpation findings
Thrills vibrate
Heaves rise & fall
Bruits indicate an obstruction
Atrioventricular valves
Rigth AV; tricuspid
Left AV; bicuspid (mitral)
Open during diastole
Semilunar valves
Between ventricles and pulmonary arteries
Pulmonic valve
Aortic valve
Open during systole
Blood flow through the heart
- Liver to right atrium (IVC)
- Right ventricle through pulmonic valve to pulmonary artery
- Lungs
- Left atrium, through mitral valve to LV
- Aorta to body
Atrial systole…
Occurs during ventricular diastole
For a moment all valves…
Are closed during isometric contraction to exceed aortic pressure
After isometric contraction
Isometric relaxation or isovolumic relaxation
Normal heart sounds
S1; AV valves close (tricuspid & mitral) to begin systole
S2; semilunar valves close (pulmonic & aortic) ending systole
Split S2; when the aortic valve closes before the pulmonic
Extra heart sounds
S3; low intense vibration (ventricles resist filling); start of diastole
“kentucky” (ventricular gallop)
S4; low frequency vibration (atrial contraction); end of diastole when ventricle is resistant to filling
“Tennessee” (atrial gallop)
S3 indicators
Left ventricular failure (ie. volume overload, HF, mitral valve regurgitation, high CO, hyperthyroidism, anemia and pregnancy)
S4 indicators
-CAD
-Cardiomyopathy with systolic overload (after load)
-LV hypertrophy
-Aortic stenosis, HTN
Respirations impact on LV systole
MoRe to the Right; inspiration increases venous return to the right side of the heart; increases stroke volume
Less to the Left; less blood is returned to the left side of the heart; decreases ventricular stroke volume
Murmurs & etiology
Turbulence
Gentle, blowing, swooshing
Conditions: Inreased velocity blood flow, decreased viscosity of blood, structural defects in valves, or unusual openings in chambers
Assessing murmurs (what to listen for)
Timing: systole or diastole
Loudness: 6 grades
Pitch
Conduction of the heart
SA node initiates (pacemaker) to AV node to bundle of His to the apex then through the ventricles
PQRST waves
P wave; depolarization of the atria
P-R interval; interval from the beginning of the P wave to the beginning of the QRS complex
QRS complex; depolarization of the ventricles
T wave; repolarization of the ventricles
Cardiac output definiton & variables
Stroke volume x HR
Variables: HR, SV, metabolic rate & O2 demand, females
Neural reflexes
Baroreceptors are pressure sensors in the aortic arch and carotid sinus that respond to BP and HR
PNS
Decreases HR
Vagal fibers release Ach
Neurotransmitters from the SNS
Increase HR
NE, E, distended radial artery
Cardiac output respiratory and metabolism
O2 demands increase in hypermetabolic states
Frank starling law
The greater the stretch (preload), the stronger the contraction and larger ejection fraction
Atrial kick does what
Augments venous return to the heart increasing ventricular volume & pressure
Compliance
More compliant ventricles mean lower filling pressure
Preload
= Volume
Inside problem
Afterload
= Constriction
Opposing pressure generated by the ventricle to open the aortic valve
Outside problem
Left ventricular outflow resistance
Aortic diastolic pressure
SVR
Aortic valve resistance
Right ventricular outflow resistance
Pulmonary artery diastolic pressure, PVR, pulmonic valve resistance
Systemic vascular resistance
Resistance of blood flow throughout systemic circulation
Peripheral vascular resistance
Resistance of blood flow throughout pulmonary circulation
Increased afterload causes & etiology
Decreases stroke volume
Caused by: HTN, aortic or pulmonic stenosis, heart O2 demand, vasoconstriction, high BMI
Decreased afterload
Increases stroke volume
Decreases ventricular work
Decreases heart O2 demand
Vasodilation
Contractility definition
Hearts abiliy to increase the extent and force of muscle fiber shortening independent of preload/afterload
Factors determing contraction/contractility
1.Altered stretching of the ventricular myocardium caused by changes in ventricular end-diastolic volume (preload)
2.Alterations in the inotropic stimulation of the ventricles
-Positive inotropic strengthens heart contraction
-Negative inotropic weakens heart contraction
3.Oxygen supply
Ejection fraction definition
Amount of blood ejected from the ventricle compared with end-diastolic volume
Ejection fraction measurments
50-70%; normal
41-49%; mild HF
<=40%; moderate HF
<=35%; severe HF
Carotid artery & jugular veins
Reflect efficiency of cardiac function
Jugular veins tell us
About right sided activity and reflect filling pressure and volume changes
Hemodynamic changes with aging
-Systolic BP increases d/t arteriosclerosis
-Left ventricular wall thickens to accommodate vascular stiffening
-Diastolic BP decreases, increasing the pulse pressure
-HR and CO do not change with aging
SVT and ventricular arrhythmias (age)
-Increase with age
-Ectopic beats are more common in older adults which can compromise CO&BP when disease is present
Tachydysrhythmias in older adults
-Not tolerated well by older adults because the myocardium is thicker and early diastolic filling is impaired at rest
-Tachycardia not tolerated well because of shortened diastole
-Compromises organs affected by aging or disease
ECG in older adults
-P-R and Q-T intervals are prolonged; QRS complex is unchanged
-Left axis deviation related to LV hypertrophy and fibrosis in the left bundle branch; increased incidence of bundle branch blockage
Common cardiac findings in infants and children
-Sinus arrhythmia; speeding and slowing of heart
-Venous hum
Deep veins
Run along deep arteries providing most of the venous return from the lower extremeties
Superficial veins
The great and small saphenous veins
Blood flows from the superficial to the deep leg veins
Perforators
connecting veins that join deep and superficial veins
Veins
Low pressure systems
Blood moves through them via: Contraction of skeletal muscle, the pressure gradient caused by breathing, and the intraluminal valves which prevent backflow
-Capacitance vessels because of their ability to stretch
Varicose veins
Have incompetent valves that cannot approximate which increases venous pressure and further dilates the vein
Lymphatic system functions
-Conserve fluid and plasma proteins that leak out of the capillaries
-Form a major part of the immune system that defends the body
-To absorb lipids from the intestinal tract
Spleen functions
-To destroy old red blood cells
-Produces antibodies
-Store red blood cells
-To filter microorganisms from the blood
Types of HTN
-Primary: Elevated BP with no specific cause
-Secondary: Elevated BP with an underlying disorder
-Complicated: Chronic HTN occuring overtime (eg. arteriosclerosis)
Hypertensive crisis
-Severe & abrupt
-Pressure impedes blood flow to cerebral capillary beds
-Hydrostatic pressure in capillaries moves vascular fluid to interstitial spaces
-Leads to cerebral edema & dysfunction
Hypertensive emergency
Develops over hours to days and has caused organ damage
Hypertensive urgency
-Develops over days to weeks and has not caused organ damage
Physical exam overview in a hypertensive crisis
Neurological dysfunction, retinal damage, pulmonary edema, HF and renal failure
Physical exam in a hypertensive crisis (CV)
-Bruits
-JVD to rule out increase volume
-Weak & thready lower extremity pulses indicating increased afterload,
-Hemodynamic instability and edema
Physical exam in a hypertensive crisis (respiratory)
-Auscultate for crackles
-Pulmonary edema
-Assess for poor oxygen exchange and signs of cyanosis
Physical exam in hypertensive crisis (renal)
-Monitor urine output, colour, frequency, and for signs of dehydration
Clinical manifestations in hypertensive crisis (neurological)
Headache, N/V, seizures, confusion, stupor, coma, encephalopathy, blurred vision and transient blindness
Hypertensive crisis (CV) can lead to…
Cardiac instability such as unstable angina to MI, pulmonary edema, and aortic dissection
Clinical manifestations in hypertensive crisis (renal)
Renal insufficiency such as decreased urine output to complete renal shutdown
Hypotension
<100/60
Inadequate tissue perfusion because of lowered CO
Shifts in intravascular volume
Hypotension manifestations
aLOC
-Chest pain (heart is pumping rapidly without being supplied with O2 and nutrients)
-Tachypnic
-Oliguria, anuria
-Lethargic
Hypotensive shock types
-Cardiogenic (heart cannot pump effectively)
-Hypovolemic
-Distributive (vasculature is not compensating for hemodynamic changes)
-Septic
-Anaphylactic
-Neurogenic
Labs to monitor for patients with HTN
-CBC
-Coagulation
-Electrolytes
-Kidney function
-Lipids
-Speciality labs: Troponin, creatinine kinase, and C-reactive protein
Labs to monitor for people with hypotension
-CBC
-Coagulation
-Electrolytes
-Kidney function
-Lipids
-Liver function
-Speciality labs (troponin, brain-natriuretic peptide, creatinine kinase, creatinine kinase of heart, C-reactive protein)
Bradycardia in pediatric population that can be lethal
-Newborns-3 years; <100bpm
-3-9 years; <60bpm
-9-16 years; <50bpm
Heart block
Impulse from SA to AV node is slowed and fails to initiate conduction
Atrial flutter
-Continuous stimuli to the AV node cannot conduct all the impulses but a few get through to the ventricle
-Only involves the atria, the venticular bundle of His is functioning normally
Atrial fibrillation
-Worse than atrial flutter
-The atria of the heart quivers
Premature ventricular contractions
-Extra contraction that originates in the ventricle
-Occasional PVC is normal, three in a row indicates that the patient has increased cardiac irritability and >10 in a minute may precipitate an MI or Vtach
-Vtach is worse than atrial flutter and atrial fibrillation
Ventricular tachycardia & K+
-Irritable focus of an impulse within the ventricle
-Life threatening and can lead to ventricular fibrillation
-Too much K+ causes cardiac irritability (decreased CO)
Ventricular fibrillation
-Quivering of the ventricle
-Impedes pumping function of the heart
-No O2 to the brain
Pertinent labs to monitor in dysrhythmia
Na+
K+; impaired kidney function (not excreting K+)
Ca+; hypocalcemia influences dysrhythmias more than hypercalcemia, increased risk for vtach
Mg+
Angina and MI primary cause
-Can be caused my atherosclerosis
Angina definition
-Diminished blood flow and lack of oxygen in the arteries in the heart leading to myocardial ischemia
Angina manifestations, precipitating factor, eventuality and types
-Chest pain
-Often occurs during activity
-Precursor to MI
-May be stable, unstable, or variant
Stable angina
-effort induced chest pain
-lasts few seconds to 15 minutes
-relieved by rest, removal of provoking factors, or NTG
Unstable angina
- lasts longer and occurs more frequently
- may be exertional or occurs at rest
- often referred to as crescendo angina, preinfarction angina, nocturnal angina
Variant (prinzmetal) angina
- chest pain that occurs at rest in early hours of the morning
- is often associated with ST segment elevations
-often cyclical
Acute MI
-Interruption of blood supply to the cardiac muscle
-Result of sustained ischemia leading to myocardial cell death
-Location of the infarction correlates with the involved coronary circulation
Causes of acute MI
-Anything impeding blood flow
-Plaque rupture
-Thrombus formation
-Coronary artery embolism
-Coronary spasm (cocaine)
-Hypotension
-Decrease in O2 delivery to tissues (anemia, shock, hypoxemia)
-Post procedure
-Spontaneous Coronary Artery Dissection
Type I MI
-Thrombosis of the coronary artery or a plaque rupture.
-Spontaneous symptoms
-Men>women
Type II MI
-Disrupted O2 supply or demand in the absence of a blockage
-Women>men
-Less chest pain and dyspnea
-May not present with ischemic events on the ECG
Angina vs acute MI discomfort
Angina; chest pain, pressure, squeezing, tightness
Acute MI; Same as angina + abdominal pain and SOB
Angina vs acute MI location and radiation
Angina; midsternal, neck, jaw, arms, and back
AMI; same as angina + increased pain and radiation
Angina vs acute MI intensity
Angina; mild-moderate
AMI; more intense, silent, and severe
Angina vs acute MI duration
Angina; 3-15 minutes
AMI; >20-30 minutes
Angina vs acute MI precipitating factors
Angina; exercise, weather, large meal, sex and stress
AMI; same as angina but may occur at rest
Angina vs acute MI associated S&S
Angina; none
AMI; Diaphoresis, SOB, abdominal pain, indigestion, fatigue, pale, tachycardia, and palpitations
Angina vs acute MI lab values
Angina; none
AMI; high sensitivity troponin, CKMB
Overview of acute MI manifestations + LV dysfunction/RV dysfunction
-Pain, ashy, clammy, cool to touch
-If LV dysfunction; crackles may be heard in the lungs
-If RV dysfunction; JVD, hepatic engorgment and peripheral edema
-Extra heart sounds
-N/V, fever
Nursing assessment of acute MI (neurological)
-Pain, anxiety, LOC, fear, pyschosocial and diaphoresis
Nursing assessment of acute MI (CV) (IPAP)
-Dysrhythmias, extra heart sounds, murmurs, cap refill, JVD, peripheral edema, BP
Nursing assessment of acute MI (respiratory)
Rate and depth, crackles (if LV involved), oxygenation
Nursing assessment of acute MI (GI)
N/V, aMotility
Nursing assessment of acute MI (renal)
Urine output
Pertinent labs to monitor with acute MI
-Hemoglobin
-Electrolytes
-Kidney function (creatinine & BUN will be high)
-Lipids & blood glucose
-Liver function tests (drawn in ALL labs)
-Troponin
-BNP (HF)
-CK-MB (only cardiac)
Types of acute MI
NSTEMI; non ST elevated MI
STEMI; ST elevated MI
Orthostatic hypotension definition
A decrease of 20 mm Hg (or more) in SBP or a decrease of 10 mm Hg (or more) in DBP
Orthostatic hypotension causes
-Intravascular volume loss (e.g., with diuretic therapy or dehydration)
-Inadequate vasoconstrictor mechanisms related to disease or medications
Unstable angina and MI diagnostic studies (not labs)
ECG
Serum cardiac markers
Coronary angiography
Paroxysmal supraventricular tachycardia (PSVT)
Dysrhythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His
Inferior wall myocardial infarction
Occurs from coronary occlusion with resultant decreased perfusion
Anterior wall myocardial infarction
Blockage in the left descending coronary artery leads to injury of the anterior myocardial tissue
Lateral wall myocardial infarction
Caused by plaque rupture with subsequent thrombus formation in the left circumflex (LCx) coronary artery or its branches
Posterior wall myocardial infarction
Thrombus in the posterior descending artery
Septal wall myocardial infarction
A patch of dying or necrotic tissue on the septum caused by delayed blood flow in the septal branch of the left anterior descending coronary artery
Etiology of pulseless electrical activity (PEA); 6 H’s & 6 T’s
Hyperkalemia, hypoxia, hypothermia, hydrogen ion excess (acidosis), hypovolemia, and hypoglycemia
-Tamponade, tension pneumothorax, thrombosis (pulmonary embolus), thrombosis (myocardial infarction), toxins, and trauma
Inferior MI
-Blockage of the right coronary artery leads to an inferior MI
-Right sided problem
Anterior MI (widow maker)
Blockage the of left anterior descending artery (LAD) leads to an anterior MI
-Left sided heart problem
Lateral wall MI
Atherosclerotic plaque rupture with thrombus formation in the left circumflex
-Left sided heart problem
Posterior MI
Occlusion of the circumflex
-Left sided heart problem
S3 means…
Left ventricular problem
STEMI is blank than NSTEMI
Worse
50ng/L of troponin
Lowest number indicating an MI
Flipped T waves
Indicate ischemia
STEMI indicates more what
Muscle damage and ST segment is elevated
ST depression and flipped T’s mean
Ischemia
ST elevation indicates
Injury
