EXAM 4 Flashcards
WEEKS 8-9 CARDIAC AND CARDIOVASCULAR DISORDERS
PRIMARY FUNCTION OF THE CIRCULATORY SYSTEM IS?
TO TRANSPORT OXYGEN AND NUTRIENTS TO THE TISSUES
WHAT IS THE CIRCULATORY SYSTEMS PARTICIPATION IN WASTE?
CARRIES WASTE FROM THE TISSUES TO THE KIDNEYS FOR ELIMINATIONS
HOW DOES THE CIRCULATORY SYSTEM CONTRIBUTE TO THE REGULATION OF BODY TEMP
THROUGH EITHER VASOCONSTRICTION OR VASODILATION TO TRANSPORT HEAT TO PERIPHERAL TISSUES WHERE IT CAN DISSIPATE INTO THE ATMOSPHERE
WHAT IS THE SIZE OF THE HEART
ABOUT THE SIZE OF YOUR FIST
HOW MUCH BLOOD DOES THE HEART TRANSPORT THROUGH THE BODY EVERY DAY
ABOUT 1800 GALLONS
WHERE IS THE HEART LOCATED
WITHIN OUR MEDIASTINUM
WHERE IS THE MEDIASTINUM LOCATED
THORACIC CAVITY
WHAT IS THE PERICARDIUM
THE LITTLE SAC THAT ENCLOSES THE HEART
2 LAYERS OF THE PERICARDIUM
VISCERAL- CLOSER TO THE HEART
PARIETAL- OUTSIDE LAYER
PERICARDIAL CAVITY
IN BETWEEN THE PERICARDIUM LAYERS
HOLDS PERICARDIAL FLUID
PERICARDIAL FLUID
SEROUS FLUID
30-50 ML
FUNCTION OF PERICARDIAL FLUID
MINIMIZE FRICTION AS THE HEART CONTRACTS AND RELAXES
PERICARDIAL EFFUSION
TOO MUCH FLUID OR FLUID BUILDUP IN THE PERICARDIAL SPACE
THE WALL (AKA MUSCLE) OF THE HEART CONSISTS OF HOW MANY LAYERS
3
ENDOCARDIUM
INNER LAYER OF THE HEART WALL INSIDE OF THE CHAMBERS OF THE HEART
3 LAYERS OF THE HEART WALL
ENDOCARDIUM
MYOCARDIUM
EPICARDIUM
MYOCARDIUM
MIDDLE LAYER OF THE HEART WALL
THICKEST/LARGEST LAYER
ACTUAL MUSCULAR LAYER OF THE HEART
EPICARDIUM
OUTER LAYER OF THE HEART
HOW MANY CHAMBERS IN THE HEART
4
WHAT ARE THE TOP CHAMBERS OF THE HEART
ATRIA (SINGULAR IS ATRIUM)
WHAT ARE THE LOWER CHAMBERS OF THE HEART CALLED
VENTRICLES
CARDIAC MUSCLE FUNCTION IS VOLUNTARY OR INVOLUNTARY
INVOLUNTARY
WHAT DOES THE CARDIAC MUSCLE RELY ON FOR CONTRACTION AND WHY
RELIANT ON EXTRACELLULAR CALCIUM FOR CONTRACTION. CARDIAC CELLS DON’T HAVE THE CAPACITY TO STORE CALCIUM WELL
HOW WOULD YOU DESCRIBE THE SKELETON OF THE HEART
LIKE A CONNECTIVE TISSUE SKELETON
SEPTUM
DIVIDES THE RIGHT AND LEFT SIDES OF THE HEART FROM ATRIA TO VENTRICLES
WHAT DOES THE CONNECTIVE SKELETON OF THE HEART PROVIDE
SUPPORT FOR THE VALVES TO HAVE SOMEWHERE TO ATTACH TO
HOW MANY VALVES ARE IN THE HEART AND WHY ARE THEY IMPORTANT
4 MAIN VALVES
HELP TO PROMOTE PROPER BLOOD FLOW DIRECTION
4 VALVES OF THE HEART
ATRIOVENTRICULAR OR AV VALVES (2)
(MITRAL VALVE AKA BICUSPID VALVE
TRICUSPID VALVE)
AND THE SEMILUNAR VALVES- AORTIC AND PULMONIC
WHAT DOES BI AND TRI DESCRIBE IN THE BICUSPID AND TRICUSPID VALVES
THE NUMBER OF CUSPS OR LEAVES THEY HAVE WHEN YOU LOOK DOWN AT THEM DIRECTLY
WHAT SUPPORTS THE VALVES IN THE HEART
PAPILLARY MUSCLES
CORDAE TENDONAE (SP?)
LONG FIBERS THAT HELP SECURE AND HOLD VALVES IN PLACE
ATRIOVENTRICULAR OR AV VALVES PREVENT BACKFLOW OF BLOOD WHEN
DURING THE SYSTOLE OR CONTRACTION OF THE HEART
SEMILUNAR VALVES
AORTIC AND PULMONIC VALVES THAT PREVENT BACKFLOW OF BLOOD FROM THE AORTA AND PULMONARY ARTERIES INTO THE VENTRICLES DURING THE DIASTOLE OR RELAXATION OF THE HEART
HOW MANY CUSPS DO THE AORTIC AND PULMONIC VALVES HAVE
3
DO WE HAVE VALVES IN OUR ATRIA WHERE BLOOD ENTERS THE HEART
NO
BECAUSE THE ATRIA HAVE NO VALVES, WHAT HAPPENS TO THE BLOOD IF THESE TOP CHAMBERS BECOME DISTENDED OR OVERFILLED WITH FLUID
IT GETS PUSHED BACK INTO THE VEINS
SPECIFICALLY PUSHED BACK INTO THE SUPERIOR VENA CAVA, INFERIOR VENA CAVA, AND POSSIBLY INTO THE JUGULAR VEINS
WHAT WILL WE SEE WHEN BLOOD BACKS UP FROM THE ATRIA
JUGULAR VEIN DISTENSION
PERIPHERAL EDEMA
SYSTOLE
PERIOD IN WHICH VENTRICLES CONTRACT
DIASTOLE
PERIOD IN WHICH VENTRICLES RELAX AND FILL
PHASES OF THE CARDIAC CYCLE
- ATRIOLE SYSTOLE BEGINS
- VENTRICULAR SYSTOLE- 1ST PHASE
- VENTRICULAR SYSTOLE- 2ND PHASE
- VENTRICULAR DIASTOLE- EARLY
- VENTRICULAR DIASTOLE- LATE
ATRIOLE SYSTOLE BEGINS
ATRIAL CONTRACTION FORCES BLOOD INTO VENTRICLES
VENTRICULAR SYSTOLE
FIRST PHASE
VENTRICULAR CONTRACTION PUSHES AV VALVES CLOSED
VENTRICULAR SYSTOLE
SECOND PHASE
SEMILUNAR VALVES OPEN AND BLOOD IS EJECTED
VENTRICULAR DIASTOLE
EARLY
SEMILUNAR VALVES CLOSE AND BLOOD FLOWS INTO ATRIA
VENTRICULAR DIASTOLE
LATE
CHAMBERS RELAX AND BLOOD FILLS VENTRICLES PASSIVELY
WHAT DOES THE CARDIAC CYCLE TELL US WHEN LOOKING AT THE SYSTOLIC AND DIASTOLIC VALUES OF BP?
DIRECT CORRELATION
ELEVATED SYSTOLIC BP INDICATES?
VENTRICLES CAN’T CONTRACT WELL BECAUSE THEY ARE HAVING TO PUSH OUT AGAINST SO MUCH PRESSURE TO PUSH THE BLOOD OUT
WHAT DOES THE ELECTRICLE CURRENT OF THE HEART ON THE EKG LINE CORRELATE TO
THE MUSCULAR CONTRACTION. THE ELECTRICAL ACTIVITY OF THE HEART GUIDES THE MUSCULAR FUNCTION OF THE HEART
ELEVATED DIASTOLIC PRESSURE INDICATES?
VENTRICLES AREN’T FULLY RELAXING SO THEY AREN’T ADEQUATELY FILLING WITH BLOOD
HOW DO WE VIEW AND MONITOR THE EKG ON A CONTINUOUS BASIS
VIA TELEMETRY OR A HARDWIRED CARDIAC MONITOR
WHAT DOES AN EKG SNAPSHOT WITH A 12 LEAD SHOW
ALLOWS YOU TO SEE IN ALL DIFFERENT AREAS OF THE HEART WHAT THE ELECTRICAL ACTIVITY IS DOING
WHERE DOES THE S1 HEART SOUND COME FROM
CLOSURE OF THE AV VALVE- SO OUR MITRAL AND TRICUSPID VALVES AT THE ONSET OF SYSTOLE
WHERE DOES THE S2 SOUND COME FROM
CLOSURE OF THE AORTIC AND PULMONIC VALVES AND MARKS THE ONSET OF DIASTOLE
IS THE HEART EVER EMPTY?
NO
AS ONE CHAMBER EMPTIES AND PUSHES BLOOD OUT, WHAT HAPPENS
MORE BLOOD IS BEING PUSHED BACK INTO IT ON THE NEXT SQUEEZE FROM A DIFFERENT CHAMBER
SVC
SUPERIOR VENA CAVA
IVC
INFERIOR VENA CAVA
HOW IS VENOUS BLOOD RETURNED TO THE HEART
FROM OUR SVC AND IVC THAT DUMPS INTO THE RIGHT ATRIUM
FROM THE RIGHT ATRIUM, WHERE DOES THE BLOOD GO
THROUGH THE TRICUSPID VALVE TO THE RIGHT VENTRICLE
WHERE DOES BLOOD GO WHEN IT LEAVES THE RIGHT VENTRICLE?
THROUGH THE PULMONARY VALVE –> THROUGH THE PULMONARY ARTERY
WHAT DOES THE PULMONARY ARTERY CARRY
DEOXYGENATED BLOOD
WHERE DOES THE PULMONARY ARTERY TAKE THE BLOOD
TO THE LUNGS
WHAT HAPPENS WHEN THE BLOOD REACHES THE LUNGS
ON A MICROSCOPIC LEVEL, THERE IS THE GAS EXCHANGE IN THE CAPILLARY NETWORK AROUND THE AVEOLI
WHAT HAPPENS WHEN BLOOD BECOMES OXYGENATED IN THE LUNGS THROUGH GAS EXCHANGE
IT COMES BACK THROUGH THE PULMONARY VEINS TO THE LEFT ATRIUM
WHAT DOES THE PULMONARY VEIN CARRY
OXYGENATED BLOOD
WHERE DOES BLOOD GO WHEN LEAVING THE LEFT ATRIUM
THROUGH THE MITRAL VALVE INTO THE LEFT VENTRICLE
WHERE DOES BLOOD GO WHEN IT LEAVES THE LEFT VENTRICLES
PASSES THROUGH THE AORTIC VALVE OUT TO THE AORTA
WHERE DOES BLOOD GO WHEN LEAVING THE AORTA
IT BRANCHES OFF INTO THE REST OF THE CIRCULATORY SYSTEM TO PERFUSE ALL TISSUES AND ORGANS OF THE BODY
WHAT DOES IT MEAN THAT THE HEART IS SELF SUFFUSING
IT ALSO HAS TO SUPPLY ITSELF WITH BLOOD
HOW DOES OUR CORONARY CIRCULATION WORK
DEOXYGENATED BLOOD FROM THE HEART COLLECTS W/IN THE CORONARY SINUS AND IS DUMPED INTO OUR SVC TO FOLLOW THE NORMAL PATHWAY
WHERE IS THE CORONARY SINUS LOCATED
THE POSTERIOR SIDE OF THE HEART
WHERE DO THE CORONARY ARTERIES BRANCH
OFF THE AORTA
HOW DOES THE HEART GET ITS BLOOD SUPPLY
BLOOD IS PUSHED THROUGH THE LEFT VENTRICLE, THROUGH THE AORTA TO SUPPLY ALL THE TISSUES, IT ALSO FEEDS ITSELF AND SUPPLIES THE CORONARY ARTERIES
LEFT MAIN CORONARY ARTERY WILL BRANCH OUT INTO WHAT
BRANCH OUT INTO THE LEFT ANTERIOR DESCENDING (LAD) AND THEN YOUR CIRCUMFLEX
CIRCUMFLEX
CURVES AROUND THE POSTERIOR SIDE OF THE HEART
LEFT CORONARY ARTERY PERFUSES WHAT
A HUGE CHUNK OF THE HEART
IF SOMEBODY HAS A CORONARY BLOCKAGE OR A MYOCARDIAL INFARCTION TO THE LEFT CORONARY ARTERY, WHAT HAS HAPPENED
CALLED A WIDOWMAKER
THERE IS A BLOCKAGE IN THE LARGE AREA SO IT ISN’T GETTING PERFUSED AND IS FATAL FOR MANY
RIGHT CORONARY ARTERY AKA RCA BRANCHES INTO WHAT
POSTERIOR DESCENDING ARTERY
WHAT IS A COMPENSATORY MECHANISM OF THE HEART IF IT REQUIRING MORE PERFUSION AND OXYGEN
THERE IS DEVELOPMENT OF COLLATERAL CIRCULATION SO OUR BODY AND OUR HEART WILL GROW ADDITIONAL VEINS AND CIRCULATION TO COMPENSATE
WHAT HAPPENS IF A PATIENT HAS A SLOW CHRONIC TYPE OCCLUSIONS
COLLATERAL CIRCULATION OVER TIME
CARDIAC OUTPUT
AMOUNT OF BLOOD PUMPED BY THE HEAERT EACH MINUTE
THE EFFICIENCY OF THE HEART
EQUATION OF CARDIAC OUTPUT
CO = SV X HR
SV AKA STROKE VOLUME
AMOUNT OF BLOOD PUMPED BY THE LEFT VENTRICLE WITH EACH CONTRACTION
NORMAL SV
60-70 ML
NORMAL CO
4-6 L/MIN
FACTORS THAT INFLUENCE CO
PRELOAD
AFTERLOAD
CONTRACTILITY
HEART RATE
PRELOAD
AMOUNT OF TENSION/STRETCH APPLIED TO HEART MUSCLE BEFORE CONTRACTION
SPECIFICALLY THE MEASURE OF FORCE ON THE ATRIA THAT ARE BEING FILLED
AFTERLOAD
AMOUNT OF FORCE/WORK THE HEART MUSCLE HAS TO APPLY TO MOVE BLOOD INTO THE AORTA
ALSO CALLED SYSTEMIC VASCULAR RESISTANCE BECAUSE PRIMARILY INFLUENCED BY BP
CONTRACTILITY
FORCE AT WHICH THE HEART CONTRACTS (HOW STRONG IS THE SQUEEZE)
HEART RATE
HOW MANY TIMES THE HEART CONTRACTS OR BEATS PER MINUTE
NORMAL EJECTION FRACTION (EF)
55-75%
WHAT DO WE SEE WITH DECREASED CARDIAC OUTPUT
S/S OF HYPOPERFUSION THAT CAN LEAD TO ORGAN DECLINE
WHY DO WE THINK OF VENOUS RETURN VOLUME WHEN WE TALK ABOUT PRELOAD
IF PATIENT IS IN FLUID OVERLOAD, THEN WE HAVE INCREASED PRELOAD BECAUSE THE ATRIA IS FILLING WITH MUCH MORE BLOOD AND THE HEART IS HAVING TO STRETCH MORE
HOW IS EJECTION FRACTION CALCULATED
SV DIVIDED BY END DISTOLIC VOLUME TO GET PERCENTAGE OF BLOOD EJECTED DURING SYSTOLE DURING THE CONTRACTION OF THE HEART
WHAT IS EF TELLING US
WHAT PERCENTAGE OF BLOOD IN THE LEFT VENTRICLE IS EJECTED AND PUSHED OUT INTO THE AORTA WITH EACH BEAT
WHEN DO WE LOOK AT EF
WHEN Tx PATIENTS WITH HEART FAILURE BECAUSE IT INDICATES FUNCTION OF THE HEART
WHAT MAKES THE HEART MUSCLE SPECIAL
IT CAN GENERATE AND RAPIDLY CONDUCT ITS OWN ELECTRICLE IMPULSES OR ACTION POTENTIALS TO EXCITE MUSCLE FIBERS AND GENERATE THE MUSCLE CONTRACTIONS
WHAT DOES CAPTURING ELECTRICAL ACTIVITY OF THE HEART IN WAVE FORM HELP DIAGNOSE
MYOCARDIAL INFARCTIONS
DYSRHYTHMIAS
OTHER CARDIAC PROBLEMS
SA NODE
SINO ATRIAL NODE
PACEMAKER OF THE HEART
PRIMARY FUNCTION: ENSURE ELECTRICAL ACTIVITY IN THE HEART IS GENERATED TO MAINTAIN 60-100 BPM
WHERE DOES ELECTRICAL ACTIVITY TRAVEL AFTER LEAVING THE SA NODE
- AV NODE (ATRIOVENTRICULAR NODE)
- DOWN TO THE FIBERS IN THE LEFT VENTRICLES
IF THERE ARE CONDUCTION ISSUES IN THE HEART, WHAT MIGHT WE SEE
FAILURE OF THE SA NODE DUE TO MYOCARDIAL INFARCTION OR OTHER REASONS
WHAT HAPPENS IF THERE IS A SA NODE DYSFUNCTION
WE HAVE A BACKUP PACEMAKER CALLED THE AV NODE BUT IT DOESN’T SEND IMPULSES AS RAPIDLY AS THE SA NODE
WHAT IS THE RATE FOR THE AV NODE
40-60 BPM
SO HEART DOESN’T BEAT AS FAST AS IT SHOULD
PERKINJE FIBERS
BACK UP TO THE BACKUP PACEMAKER
CAN GENERATE THEIR OWN ELECTRICAL IMPULSES AT 15-40 BPM (SEVERE BRADYCARDIA)
MINOR ISSUES OF CARDIAC CONDUCTION
PREMATURE BEATS
LATE BEATS
LITTLE PALPITATIONS
RAPID RHYTHMS
TACHYDYSRHYTHMIAS
FAST HEART RHYTHM
BRADYDISRHYTHMIAS
SLOW HEART RHYTHM
DISORGANIZED ELECTRICAL ACTIVITY
TOP CHAMBERS ARE NOT BEATING EFFECTIVELY WITH THE BOTTOM CHAMBERS SO THEY ARE NOT IN TIME
TO HAVE ADEQUATE BLOOD FLOW, WE HAVE TO HAVE A GOOD SYSTEM OF WHAT
PATENT BLOOD VESSELS AND ADEQUATE PERFUSION PRESSURE
HOW MANY LAYERS ARE IN THE WALLS OF BLOOD VESSELS (WITH EXCEPTION OF THE CAPILLARIES)
3
3 LAYERS OF BLOOD VESSELS
TUNICA EXTERNA-OUTER
TUNICA MEDIA-MIDDLE
TUNICA INTIMA-INNER
HOW ARE CAPILLARY LAYERS DIFFERENT THAT BLOOD VESSELS
HAVE VERY THIN LAYERS OF ENDOTHELIAL CELLS BECAUSE THIS ALLOWS FLUID/GASES/NUTRIENTS TO PASS
WHAT ARE BLOOD VESSELS COMPOSED OF
ENDOTHELIAL CELLS THAT ALLOW FOR THEM TO HAVE A SEMI PERMEABLE MEMBRANE
WHAT IS THE TUNICA MEDIA COMPOSED OF
SOME VASCULAR SMOOTH MUSCLE CELLS WHICH GIVES THE ABILITY TO CONSTRICT OR DILATE IN RESPONSE TO OUR SYMPATHETRIC NERVOUS SYSTEM ACTIVATION AND OTHER HOMEOSTATIC MECHANISMS
WHAT ARE MOST DIFFERENCES OF ARTERIAL AND VENOUS CIRCULATION DUE TO
STRUCTURE OF THE VESSELS
WHAT THEY ARE CARRYING
AMOUNT OF PRESSURE
CHARACTERISTICS OF ARTERIAL CIRCULATION
- THICKER VESSELS
- ELASTIC
- OXYGENATED BLOOD
- HIGH PRESSURE SYSTEM
CHARACTERISTICS OF VENOUS CIRCULATION
- THIN WALLED VESSELS
- DISTENSIBLE
- COLLAPSIBLE
- DEOXYGENATED BLOOD
- LOW PRESSURE SYSTEM
- VALVES
- MUST OPPOSE GRAVITY
DO YOU BLEED OUT FASTER IF A CUT IS ARTERIAL OR VENOUS
ARTERIAL BECAUSE OF HIGH PRESSURE
PULSATILE
VERY HIGH PRESSURE
IS VENOUS BLOOD COMPLETELY DEOXYGENATED
NO
DO VEINS HAVE A PULSE
NO
FACTORS AFFECTING BLOOD FLOW
- ADEQUATE BLOOD VOLUME
- PRESSURE/RESISTANCE IN VASCULATURE
- RADIUS OF BLOOD VESSEL
- VELOCITY OF FLOW
- LAMINAR/TURBULENT FLOW
- DISTENTION AND COMPLIANCE
ATHEROSCLEROSIS AND BLOOD FLOW
IT IS HARDENING OF THE ARTERIES SO MORE PRESSURE AND RESISTANCE RESULTING IN LOW BLOOD FLOW
ATHEROSCLEROTIC PLAGUES AND BLOOD FLOW
IS A BUILDUP OF FATTY PLAQUES WITHIN THE BLOOD VESSEL (OR COULD EVEN HAVE VASOCONSTRICTION) CAUSING VESSEL SHRINKING AND LESS FLOW
VELOCITY OF BLOOD FLOW
DEPENDS ON HR AND FORCES THAT ARE ACTING ON THE VESSEL. LOW VELOCITY = LOW FLOW
LAMINAR FLOW
NORMAL FLOW: THIN LAYER OF PLASMA ADHERES TO VESSEL WALL AND LAYERS OF BLOOD CELLS AND PLATELETS SHEAR AGAINST IT. EACH LAYER TOWARDS THE MIDDLE MOVES FASTER THAN PREVIOUS LAYER.
IF WE DON’T HAVE BLOOD FLOWING IN THE CORRECT DIRECTION, IT DECREASES SPEED AND FLOW
HOW MUCH MORE DISTENDABLE ARE VEINS THAN ARTERIES
ABOUT 24 TIMES
MECHANISMS THAT REGULATE BP
SYMPATHETIC NS
RAAS
INFLAMMATORY RESPONSE
CLOTTING
SYMPATHETIC NS
EPINEPHRINE AND NOREPINEPHRINE (NEUROTRANSMITTERS) REGULATE BY SEVERAL MECHANISMS
HOW DO EPINEPHRINE AND NOREPINEPHRINE REGULATE BP
- CONTROL RELEASE OF RENIN FROM KIDNEYS TO ACTIVATE RAAS TO INCREASE BP
- CAUSE VASOCONSTRICTION THAT INCREASES BP
RAAS AKA RENIN ANGIOTENSIN ALDOSTERONE SYSTEM
ANGIOTENSIN II (MOST POWERFUL VASOCONSTRICTOR IN BODY) THAT INCREASES BP
ANGIOTENSIN II ALSO STIMULATE ADRENAL GLANDS (LOCATED ON TOP OF KIDNEY) TO RELEASE ALDOSTERONE
ALDOSTERONE
- CAUSES KIDNEYS TO REABSORB SODIUM
- REABSORBTION OF SODIUM MEANS REABSORBTION OF WATER WHICH CAUSES EXCRETION OF POTASSIUM
INFLAMMATORY RESPONSE AND REGULATION OF BP
HISTAMINE, BRADYKININ, PROSTAGLANDINS ALL CAUSE VASODILATION TO DECREASE BP
CLOTTING AND BP REGULATION
SEROTONIN THAT IS TRANSPORTED BY PLATELETS AND AIDS IN CLOTTING AND CAUSES VASOCONSTRICTION AS WELL AS AIDING PLATELET AGGREGATION WHICH INCREASES BP
VASOPRESSIN AND BP REGULATION
AKA ADH
STIMULATES BODY TO HOLD ONTO OUR VOLUME VS RELEASING FLUID. MORE VOLUME = HIGHER BP
ADEQUATE PERFUSION REQUIRES 4 KEY ELEMENTS
- PUMPING ABILITY OF THE HEART
- INTACT VASCULAR SYSTEM TO TRANSPORT BLOOD
- SUFFICIENT BLOOD TO FILL THE VASCULAR SYSTEM
- TISSUES THAT CAN EXTRACT O2 AND NUTRIENTS
WHAT HAPPENS WHEN THERE IS DYSFUNCTION IN THE CIRCULATORY SYSTEM
- INTERRUPTION OF CORONARY CIRCULATION
- BP CHANGES
- ELECTRICAL CONDUCTION PROBLEMS
- VALVE PROBLEMS
S/S OF INTERRUPTION OF CORONARY CIRCULATION
MYOCARDIAL INFARCTION
CHEST PAIN/ANGINA
THE ____ IS THE MAIN ORGAN OF THE CARDIOVASCULAR SYSTEM
HEART
WHAT IS THE MEDICAL TERM FOR HIGH BP
HYPERTENSION
WHICH IS RESPONSIBLE FOR REGULATING HEART RATE?
A. PURKINJE FIBERS
B. SA NODE
C. BUNDLE OF HIS
D. AV NODE
B
THE ________ ARE THE LOWER CHAMBERS OF THE HEART
VENTRICLES
THE _______ IS THE LARGEST ARTERY IN THE BODY
AORTA
THE CARDIOVASCULAR SYSTEM IS RESPONSIBLE FOR TRANSPORTING O2, NUTRIENTS, AND HORMONES THROUGHOUT THE BODY.
T/F
TRUE
WHAT IS THE AVERAGE RESTING HEART RATE FOR ADULTS
60-100 BPM
CARRIES OXYGENATED BLOOD FROM THE HEART TO THE REST OF THE BODY
AORTA
CARRIES DEOXYGENATED BLOOD FROM THE HEART TO THE LUNGS
PULMONARY ARTERY
MICROSCOPIC BLOOD VESSELS WHERE GAS EXCHANGE OCCURS
CAPILLARIES
CARRIES BLOOD BACK TO THE HEART
VEINS
WHICH CHAMBER OF THE HEART RECEIVES OXYGENATED BLOOD FROM THE LUNGS
LEFT ATRIUM
WHAT IS THE ROLE OF VALVES IN THE CARDIOVASCULAR SYSTEM
TO PREVENT BACKWARD FLOW OF BLOOD
SYSTOLIC PRESSURE
VENTRICULAR CONTRACTION
DIASTOLIC PRESSURE
VENTRICULAR RELAXATION
MEAN ARTERIAL PRESSURE
TISSUE PERFUSION
PULSE PRESSURE FORMULA
SYSTOLIC - DIASTOLIC
CARDIAC OUTPUT FORMULA
HR X SV
MAP FORMULA
DIASTOLIC + (PULSE PRESSURE/3)
BLOOD PRESSURE FORMULA
CO X TOTAL PERIPHERAL RESISTANCE
CARDIOVASCULAR CENTER
MECHANISMS FOR BP REGULATION
MEDULLA
PONS
NEURAL MECHANISMS
MECHANISMS FOR BP REGULATION
- ANS–> SYMPATHETIC, PARASYMPATHETIC
- BARORECEPTOR AND CHEMORECEPTOR REFLEXES
HUMORAL MECHANISMS
MECHANISMS FOR BP REGULATION
NATRIURETIC PEPTIDES
RAAS
SYMPATHETIC NS
ADH
PRIMARY/ESSENTIAL HYPERTENSION
90-95% OF CASES
NO CAUSE CAN BE IDENTIFIED
SECONDARY HYPERTENSION
ELEVATION IN BP DUE TO ANOTHER DISEASE LIKE RENAL DISEASE, DISORDERS OF ADRENAL HORMONES, PHEOCHROMOCYTOMA
5-10% OF CASES
HYPERTENSIVE CRISIS
SYSTOLIC > 180
AND/OR
DIASTOLIC >120
ORTHOSTATIC (POSTURAL) HYPOTENSION
DROP IN BP WHEN MOVING FROM A SEATED OR SUPINE POSITION
DROP IS 20MMHG SYSTOLIC OR 10 MMHG DIASTOLIC OR MORE
RISK FACTORS OF BP ISSUES
AGE, GENDER, RACE, FAMILY Hx, DIET, DYSLIPIDEMIAS, TOBACCO, ETOH, FITNESS, OBESITY, METABOLIC ABNORMALITIES, SLEEP APNEA
If I move too quickly from a reclining to standing position,what does my baroreceptor reflex do
Your baroreceptor reflex is a series of quick actions your body takes to keep your blood pressure in a normal range in response to an abrupt change in position
IF YOU MOVE FASTER THAN THIS HOMEOSTATIC MECHANISM CAN RESPOND, YOUR BP WILL DROP
If natriuretic peptide is released, what will happens to B/P?
THERE IS A FALL IN BP
What two actions occur in response to the release of angiotensin II?
VASOCONSTRICTION AND STIMULATION OF THE SYMPATHETIC NS TO RAISE BP
If cardiac output increases what happens to blood pressure?
BP RISES
If I infuse fluids or blood what happens to venous volume?
What determinant of cardiac output is affected?
THERE IS AN INCREASE IN VENOUS VOLUME. THIS AFFECTS PRELOAD, AND VENOUS RETURN, AS WELL AS HEART RATE AND STROKE VOLUME
What happens to blood pressure in response to massive vasodilation?
DECREASED BP BECAUSE VASODILATION CAUSES DECREASE IN SVR AND INCREASE IN BLOOD FLOW
What effect does arterial vasoconstriction have on blood pressure?
IT REDUCES VOLUME IN THE BLOOD VESSEL, SO FLOW IS REDUCED CAUSING HIGHER RESISTANCE AND HIGHER BP
NORMAL BP
LESS THAN 120/ LESS THAN 80
ELEVATED BP
120-129/LESS THAN 80
HYPERTENSION STAGE 1
130-139/80-89
ONLY NEED ONE
HYPERTENSION STAGE 2
> 140/>90
ONLY NEED ONE
HYPERTENSIVE CRISIS
> 180/>120
CAN BE ONE OR BOTH
WHAT IS THE GOAL OF HYPERTENSION Tx
BP LESS THAN 130/80
HYPERTENSION Tx
WEIGHT
SODIUM
DASH DIET
ETOH
EXERCISE
SMOKING CESSATION
MAINTAIN Ca AND K INTAKE
MEDICATIONS
DASH DIET
DIETARY APPROACHES TO STOP HYPERTENSION
FLEXIBLE AND BALANCED EATING PLAN THAT HELPS CREATE A HEART HEALTHY EATING STYLE FOR LIFE
ETOH
ETHYL ALCOHOL
ALCOHOL CONSUMPTION
EFFECTS OF HYPERTENSION ON THE HEART
HYPERTROPHY
ANGINA
MI
HEART FAILURE
EFFECTS OF HIGH BP ON THE BRAIN
STROKE
TIA
OTHER EFFECTS OF HYPERTENSION
CHRONIC KIDNEY DISEASE
PERIPHERAL VASCULAR DISEASE
RETINOPATHY
SEXUAL DYSFUNCTION
A patient complains of dizziness andlightheadedness upon getting up in the morningWhat problem does the nurse suspect?
ORTHOSTATIC HYPOTENSION
Give three examples of target organ damage thatcan occur in association with uncontrolledhypertension?
CHRONIC KIDNEY DISEASE
BRAIN-STROKE, TIA
HEART- HEART FAILURE, MI, ANGINA
A client has had repeated B/P ranging from 140-159/90-99. What is the B/P classification?
HYPERTENSION STAGE 2
A client presents to the Emergency Room with a B/P of 210/110 and complaints of a headache. What problem is represented?
HYPERTENSIVE CRISIS
What is the treatment for hypertension?
SMOKING CESSATION
WEIGHT LOSS
MEDS
DASH DIET
Na, Ca, AND K CONTROL
CONTROL ALCOHOL CONSUMPTION
FUNCTIONS OF THE ENDOTHELIUM
PART 1
Selectively permeable barrier
Modulates blood flow and vascular reactivity
Regulates thrombosis
Regulates cell growth
FUNCTIONS OF THE ENDOTHELIUM
PART 2
Regulates inflammatory/immune response
Maintains extracellular matrix
Involved in the metabolism of lipoproteins
ENDOTHELIAL DYSFUNCTION
changes inthe normal function in response to smoking, dys/hyperlipidemia, diabetes and obesity
What are lipids?
Cholesterol, triglycerides
any of a class of organic compounds that are fatty acids or their derivatives and are insoluble in water but soluble in organic solvents. They include many natural oils, waxes, and steroids.
What are lipoproteins?
any of a group of soluble proteins that combine with and transport fat or other lipids in the blood plasma.
Carriers of lipids in the blood
WHAT ARE APOLIPOPROTEINS
Protein combines with a lipid toform a lipoprotein. Promotesmovement of lipids in bloodand between cells
A is a protein carried in HDL (“good”) cholesterol. It helps start the process for HDL to remove bad types of cholesterol from your body
What are the five types of lipids?
Chylomicrons, VLDL, IDL,HDL, LDL
Dyslipidemia
Dyslipidemia is the imbalance of lipids such as cholesterol, low-density lipoprotein cholesterol, (LDL-C), triglycerides, and high-density lipoprotein (HDL)
Lipoprotein Structure
Lipoproteins are complex particles that have a central hydrophobic core of non-polar lipids, primarily cholesterol esters and triglycerides. This hydrophobic core is surrounded by a hydrophilic membrane consisting of phospholipids, free cholesterol, and apolipoproteins
HDL AND LDL AFFECT ON ATHEROSCLEROSIS
HDL lowers risk of atherosclerosis, LDL increases risk
CORE LIPID OF VLDL
TRIGLYCERIDE
CORE LIPID OF LDL AND HDL
CHOLESTEROL
APOLIPOPROTEIN OF VLDL
B-100
E
OTHERS
APOLIPOPROTEIN OF LDL
B-100
APOLIPOPROTEIN OF HDL
A-I
A-II
A-IV
TRANSPORT FUNCTION OF VLDL
DELIVERS TRIGLYCERIDES TO NON-HEPATIC TISSUES
TRANSPORT FUNCTION OF LDL
DELIVERS CHOLESTEROL TO NON-HEPATIC TISSUES
TRANSPORT FUNCTION OF HDL
TRANSPORTS CHOLESTEROL FROM NON-HEPATIC TISSUES AND BACK TO LIVER
INFLUENCE OF VLDL ON ATHEROSCLEROSIS
PROBABLE CONTRIBUTOR
INFLUENCE OF LDL ON ATHEROSCLEROSIS
DEFINITE CONTRIBUTOR
INFLUENCE OF HDL ON ATHEROSCLEROSIS
PROTECTS AGAINST
LDL CHOLESTEROL LABS
<100 = OPTIMAL
100-129 = NEAR/ABOVE OPTIMAL
130-159 = BORDERLINE HIGH
160-189 = HIGH
>190 = VERY HIGH
TOTAL CHOLESTEROL LABS
LESS THAN 200 = DESIRABLE
200-239 = BORDERLINE HIGH
240 OR HIGHER = HIGH
HDL CHOLESTEROL LABS
LESS THAN 40 = LOW
HIGHER THAN 60 = HIGH
HYPERCHOLESTEROLEMIA
HIGH CHOLESTEROL
Atherosclerosis
Accumulation of fibrofatty material in intimal artery wall (large, medium arteries)
ATHEROSCLEROSIS CAN LEAD TO WHAT
PERFUSION PROBLEMS
CAD
PAD
STROKE
ATHEROSCLEROSIS PROGRESSION
- endothelial injury monocytes, inflammatory cells migrate
- inflammation, foam cell formation, lipid deposits, fibrous caps
- plaque with a lipid core, calcified lesion- susceptible to rupture, bleeding, thrombus formation
PROGRESSES WITH AGE
common sites of Atherosclerosis
Atherosclerosis can affect most of the arteries in the body, including arteries in the heart, brain, arms, legs, pelvis, and kidneys.
risk factors of Atherosclerosis
High cholesterol and triglyceride levels.
High blood pressure.
Smoking.
Type 1 diabetes.
Obesity.
Physical inactivity.
High saturated fat diet
Clinical manifestations of atherosclerosis
Usually none until severe narrowing, blocking of the artery, decreased perfusion
complications of atherosclerosis
Rupture, thrombus formation –> ischemia, injury, infarction of cells (peripheral, brain, coronary arteries)
Aneurysm
3 lesions of atherosclerosis
fatty streaks
fibrous plaques
complicated lesions
fatty streak Atherosclerosis
Fatty streaks appear when the presence of foam cells at the site of plaque formation expands. At this stage, a lipid core has been formed that will progress into a mature atherosclerotic plaque following additional influx of different inflammatory cell types and extracellular lipids.
complicated lesions of Atherosclerosis
complex plaque referred to as complicated fibroatheromatous plaques or complex lesions. Characterized by possible surface defect, hemorrhage with or without bleeding, and visible lipid and collagen deposits plus thrombotic materials.
fibrous plaque atherosclerosis
Atherosclerotic plaque begins as fibrous plaque. This consists of an amorphous central lipid core of cellular debris, cholesterol, cholesterol esters, and foam cells. A fibrous cap surrounds the fibrous plaque, consisting mainly of smooth-muscle cells in a matrix of collagen and proteoglycans.
What are the risk factors for endothelial dysfunction?
diabetes, dyslipidemia, hypertension, smoking, aging, and obesity
What are the five types of lipoproteins?
chylomicrons
very-low-density lipoproteins (VLDL)
intermediate-density lipoproteins (IDL)
low-density lipoproteins (LDL),
high-density lipoproteins (HDL)
Which lipoprotein primarily carries cholesterol?
LDL
which lipoprotein primarily carries triglycerides
VLDL
Which lipoprotein carries cholesterol from the tissues to the liver?
HDL
What is an optimal LDL, HDL, total cholesterol?
our HDL (“good” cholesterol) is the one number you want to be high (ideally above 60). Your LDL (“bad” cholesterol) should be below 100. Your total should be below 200.
What are the three types of atherosclerotic lesions?
FATTY STREAKS
FIBROUS PLAQUES
COMPLICATED LESIONS
How can I modify hypertension and diabetes and reduce the risk of atherosclerosis?
SMOKING CESSATION
EXERCISE
MAINTAIN HEALTHY WEIGHT
EAT HEALTHY
MANAGE STRESS
Arterial Disease - Extremities
PERIPHERAL ARTERY DISEASE
THROMBOANGIITIS OBLITERANS AKA BEURGER DISEASE
RAYNAUD PHENOMENON
PERIPHERAL ARTERY DISEASE
ATHEROSCLEROTIC BLOCKAGES
LARGE ARTERIES (NOT HEART, BRAIN, AORTIC ARCH)
Thromboangiitis obliterans (Buerger disease)
non-sclerotic inflammation and thrombosis
small and medium sized arteries and veins in foot and lower leg
RAYNAUD PHENOMENON
intense vasospasm
arteries and arterioles in fingers and occassionally. toes
Patho of Peripheral Artery Disease
Patho: atherosclerosis, or inflammatory process
risks of peripheral artery disease
advancing age
smoking
diabetes
onset of peripheral artery disease
gradual
clinical manifestations of peripheral artery disease
ntermittent claudication (calf pain with walking), thinning of skin, decrease in size of leg muscles, numbness, leg color- dependent rubor, blanches with elevation, cool, weak or absent pulses, ulceration, gangrene
diagnosis of peripheral artery disease
physical exam
us
mri
angiography
bp
Tx of peripheral artery disease
decrease risk and symptoms
Thromboangiitis Obliterans (Buerger Disease)
basic info
Non-sclerotic, inflammatory disorder —> thrombosis of small and medium sized arteries and veins usually in feet, lower legs
cause of Thromboangiitis Obliterans (Buerger Disease)
unknown
risk factors of Thromboangiitis Obliterans (Buerger Disease)
less than 35 yo
heavy smoker
genetics
Tx of Thromboangiitis Obliterans (Buerger Disease)
smoking cessation
meds
surgery
diagnosis of Thromboangiitis Obliterans (Buerger Disease)
ankle/arm ratio
us
mri
ct
arteriography
clinical manifestations of Thromboangiitis Obliterans (Buerger Disease)
pain (arch of foot), intermittent claudication, increased sensitivity to cold, decreased pulses, thin shiny skin, with impaired hair/nail growth, tissue
Raynaud Phenomenon
basic info
Vasospasm – arteries, arterioles, usuallyoccurs in hands/fingers
Raynaud Phenomenon
cause
unknown
Raynaud Phenomenon
risk factors
young women
cold exposure
strong emotions
Raynaud Phenomenon
clinical manifestations
pallor
cyanosis
hyperemia
normal color
cold
numbness
paresthesias
Raynaud Phenomenon
diagnosis
cold water immersion of hands
doppler studies
Raynaud Phenomenon
treatment
eliminate cause
meds
surgery
aneurysms
basic info
Localized area of vessel dilation caused by weakness in arterial wall
types of aneurysms
berry
fusiform
dissecting (life threatening)
aneurysms
clinical manifestations
depends on location and size
aneurysms
diagnosis
mri
ct
us
aneurysms
treatment
reduce risk of rupture
surgical intervention
aaa size (cm) compared to annual risk of rupture (%)
less than 3.0 = 0%
3.0-3.9 = 0.4%
4.0-4.9 = 1.1%
5.0-5.9 = 3.3%
6.0-6.9 = 9.4%
7..0-7.9 = 24%
endovascular aortic repair
evar
an important advance in the treatment of abdominal aortic aneurysm (AAA). EVAR is performed by inserting graft components that are folded and compressed within a delivery sheath through the lumen of an access vessel, usually the common femoral artery.
A client complains of pain in the calf when walking. The nurse understands this to be a symptom of what disorder?
claudication is a symptom of PAD
what causes claudication in PAD
The pain is caused by too little blood flow to the legs or arms.
What arterial disorder primarily manifests in the hands and fingers?
raynaud’s phenomenon
What advice to reduce the risk of Raynaud’s phenomenon would you provide to a client?
avoid prolonged exposure to cold
avoid sudden temp changes
smoking cessation
treat secondary diseases
What advice to reduce the risk of Buerger’s disease would you provide to a client?
avoid nicotine
smoking cessation
meds usually don’t work
Where do berry aneurysms commonly occur?
on arteries at the base of the brain
most common type of aneurysm
What is the risk of an aneurysm that is increasing in size
they are at high risk for rupture
venous disorders
varicose veins
chronic venous insufficiency
venous thrombosis
varicose veins
location
Primary (superficial veins), secondary disorders (deep veins)
varicose veins
risk factors
prolonged standing, gender, age, obesity, increased intra-abdominal pressure, heavy lifting, pregnancy
vericose veins and prolonged increased venous pressure
leads to venous dilation and valve incompetence
varicose veins
clinical manifestations
aching, edema, warmth, physical look –redness, ropiness of veins
varicose veins
complications
can lead to venous insufficiency
varicose veins
diagnosis
physical exam
doppler studies
angiographic venous studies
varicose veins
treatment
improve flow, prevent injury
– Compression/support stockings
– Sclerotherapy - superficial
– Surgical treatment
venous insufficiency
clinical manifestations
venous hypertension
edema
varicose veins
skin changes and discoloration
skin ulceration
Venous Thrombosis - Thrombophlebitis
basics
virchow’s triad- risks
1. venous stasis
2. increased blood coagulability
3. vascular wall injury
*immobilization
Venous Thrombosis - Thrombophlebitis
clinical manifestations
pain (calf, distal thigh, popliteal areas), swelling, deep muscle tenderness, some are asymptomatic
Venous Thrombosis - Thrombophlebitis
diagnosis
us
venography
labs- d dimer
Venous Thrombosis - Thrombophlebitis
complications
pulmonary embolism
Venous Thrombosis - Thrombophlebitis
treatment
Prevention
Thrombolytics, anticoagulation,
Bedrest – gradual ambulation with support stockings (avoid standing, sitting)
What are the three elements of Virchow’s triad?
These are endothelial injury, venous stasis, and hypercoagulability
With venous disorders will clients lack a pulse?
possibly
Why are nurses at risk for the development of varicose veins?
long shift
heavy lifting
constantly on feet
Why do venous stasis ulcers develop?
Venous ulcers typically occur because of damage to the valves inside the leg veins. These valves control the blood pressure inside the veins. They allow it to drop when you walk. If the blood pressure inside your leg veins doesn’t fall as you’re walking, the condition is called sustained venous hypertension.
What complication is a client with a deep vein thrombosis at risk for?
pulmonary embolism (PE)
Tests Used in Assessment of Coronary Blood Flow and Perfusion
ekg
stress test
echocardiography
cardiac catheterization and arteriography
Electrocardiography (EKG) –
measures electrical activity of the heart-
ambulatory EKG monitoring –
Holter monitor
stress testing
monitors cardiac function under stress (exercise, pharmacologic)
echocardiography
assessment of structure, function of the heart using ultrasound
Cardiac catheterization and arteriography –
catheter advanced into the heart
– Right heart – vein views great vessels,chambers
– Left heart – artery uses dye to viewcoronary vessels
Acute Pericarditis
Inflammation of the pericardium
Acute Pericarditis
causes
infectious, non-infectious process
Acute Pericarditis
patho
vasodilation, increased capillary permeability, WBC’s, exudate in pericardial space
Acute Pericarditis
clinical manifestations
chest pain – pleuritic/positional fever, pericardial friction rub, EKG changes
Acute Pericarditis
diagnosis
ekg
echo
cxr
labs
Acute Pericarditis
treatment
based on cause
Acute Pericarditis
complications
recurrence, pericardia leffusion, pericardial tamponade, adhesions/scar tissue
Pericardial effusion
– accumulation of fluid in pericardialcavity
Pericardial tamponade
– life threatening compression of the heart due to blood/fluid in pericardial space
Pericardial Effusion/Tamponade
diagnosis
echo
ekg
Pericardial Effusion/Tamponade
treatment
pericardiocentesis
Pericardial Effusion/Tamponade
clinical manifestations
jugular vein distention, narrowing of pulse pressure, muffled heart sounds, tachycardia, pulsus paradoxus (fall in B/P with inspiration)
Coronary Artery Disease
Disease of heart as a result of impaired coronary blood flow
* Two main coronary arteries branch off the aortic root
* Most common cause of CAD is atherosclerosis.
coronary artery disease
complications
myocardial ischemia, angina, MI, arrhythmias, heart failure, sudden death
What normally happens in a blood vessel when oxygen demand exceeds supply
A mismatch between myocardial oxygen supply and demand can result in myocardial ischemia or infarct. Unfortunately, infarct results in irreversible damage to the myocardium
What normally happens in a blood vessel when oxygen supply cant meet demand
If your blood has low levels of oxygen, it can’t deliver enough oxygen to your organs and tissues that need it to keep working (hypoxia). This can damage your heart or brain if it persists over time
- Chronic ischemic heart disease
cad
arrowing of artery –> atherosclerosis or vasospasm –>Recurrent, transient
- Acute coronary syndrome
CAD
Disruption of atherosclerotic plaque –> unstable angina, MI
plaque
CAD
– Stable, fixed – obstructs flow
– Unstable – obstructs flow, risk for rupture, seen in ACS
- Thrombosis, vessel occlusion
CAD
Platelet aggregation, thrombus formation
Atherosclerotic Plaque – Stable,
Stable atherosclerotic plaque builds up over time and causes arteries to become hardened. It can lead to narrowing of the arteries over time, so much so that eventually blood flow to the heart and other organs is restricted. This obstructive stable plaque can be detected and treated.
Atherosclerotic Plaque – unstable
Instability of coronary atherosclerotic plaque culminates in abrupt vascular thrombus formation that impedes blood flow and leads to critical myocardial ischemia. Clinically, this often manifests as life-threatening Acute Coronary Syndromes (ACS)
Chronic Ischemic Heart Disease
Blood supply does not meet demand
* Causes: Atherosclerosis, vasospasm
Chronic Ischemic Heart Disease
types
– Chronic stable angina/exertional
– Variant (vasospastic)
– Silent ischemia
– Chest pain with normal coronary angiography
– Ischemic cardiomyopathy
Chronic Ischemic Heart Disease –Chronic Stable Angina
Fixed plague – disparity between supply/demand*
Angina = pain- not all cad patients have pain
Chronic Ischemic Heart Disease –Chronic Stable Angina
causes
ncreased demand – cold, exertion, stress
Chronic Ischemic Heart Disease –Chronic Stable Angina
location of pain
Substernal area, may radiate to back, left shoulder, jaw, arms
Chronic Ischemic Heart Disease –Chronic Stable Angina
Tx
relieved with rest
nitroglycerin
Silent myocardial ischemia
Chronic Ischemic Heart Disease -
impaired blood flow in the absence of pain
Variant (vasospastic) angina –
Chronic Ischemic Heart Disease -
hypercontractility of vascular smooth muscle, occurs at rest with minimal exercise, frequently during night, EKG changes and dysrhythmias
Chest pain with normal coronary angiography –
cardiac syndrome X, ?? Cause
Ischemic cardiomyopathy
– CAD from myocardial dysfunction
Diagnosis/Treatment: Chronic Ischemic Disease
part 1
History/physical – risk factors, pain -characteristics
* Lab studies – lipid panel, biomarkers are normal
* Diagnostic tests – EKG, echo, stress testing, CT, MRI, cardiac cath
Diagnosis/Treatment: Chronic Ischemic Disease
part 2
reduce symptoms,
prevent MI
– Pharmacologic – meds
– Coronary interventions – PCI (angioplasty, stent placement), CABG
– Non-pharmacologic – reduce risk factors
What are two modifiable risk factors associated with coronaryartery disease?
smoking
diabetes
obesity
diet
stress
What are two unmodifiable risk factors associated with coronaryartery disease?
gender
race
family Hx
advancing age
Which type of angina is caused by vasospasm?
Prinzmetal angina (vasospastic angina or variant angina) is a known clinical condition characterized by chest discomfort or pain at rest with transient electrocardiographic changes in the ST segment, and with a prompt response to nitrates. These symptoms occur due to abnormal coronary artery spasm.
What would you advise a client who experiences angina while walking to do?
stop and rest
What problem other than atherosclerosis can cause chronic ischemic heart disease?
Obesity, limited physical activity, psychosocial factors such as stress and depression, as well as co-existing chronic kidney disease or another atherosclerotic cardiovascular disease (ASCVD) such as stroke, or peripheral vascular disease (PVD) are also associated with ischemic heart disease.
What medication is commonly used to reduce the symptoms of angina?
sublingual nitroglycerin
Acute Coronary Syndrome (ACS) -
types
unstable angina
non st segment elevation (non q wave) mi
st segment elevation MI (STEMI)
unstable angina
acs
- Ischemia
- No elevation in biomarkers, some EKG changes
- Non-ST segment elevation (non-Q wave) MI
Acute Coronary Syndrome (ACS) -
- Severe ischemia with myocardial damage
- Biomarker elevation, no ST elevation on EKG, some changes
- ST segment elevation MI (STEMI)
Acute Coronary Syndrome (ACS) -
- Ischemic death of myocardial tissue
- Biomarker elevation, ST elevation on EKG
ACS Unstable Angina/Non-ST MI
patho
- Development of unstable plaque
– Rupture, non-occlusive thrombus formation - Obstruction by spasm, constriction
- Severe narrowing of the coronary lumen
- Inflammation
- Physiologic state causing ischemia related to decreased O2 supply
ACS - Unstable Angina, Non ST MI Pain in Contrast to Stable Angina
- Pain with UA, Non ST MI
– Occurs at rest or with minimal exertion
– Lasts more than 20 minutes if untreated
– Severe – described as frank pain, of new onset
– More severe, prolonged, or frequent than previously experienced.
ACS - STEMI
patho part 1
- Lack of blood flow to heart* Aerobic to anaerobic metabolism–>inadequate energy to sustain cell function
- Loss of contractile function
- Cell changes in minutes
ACS-STEMI
PATHO PART 2
- Loss of function of ischemic area
- Irreversible damage-40 minutes of severei schemia
- Necrosis 20-40 minutes following severe ischemia
- Recover related to size, location of MI
Evaluation of ACS (UA, Non-ST, STEMI)
- Diagnostics
- EKG changes – electrical conduction changes through damaged tissue
- ECHO –wall motion abnormalities
- Serum biomarkers (labs)
Evaluation of ACS (UA, Non-ST, STEMI)
DIAGNOSTICS-SERUM BIOMARKERS LABS
- Troponin I (TnI)
- Troponin T (TnT)
- Creatine kinase (CK-MB)
- Myoglobin
STEMI (ACS)
Clinical Manifestations –
- Chest pain – abrupt onset, or progression from UA/NSTEMI
– Severe, unrelieved, may radiate to jaw, shoulder, upper back, arm - Nervous system responses
- Hypotension, shock (cardiogenic – pump failure) ,dysrhythmias
STEMI (ACS)
NERVOUS SYSTEM RESPONSES
– GI distress, nausea, vomiting
– Tachycardia, vasoconstriction
– Anxiety, restlessness, impending doom
ACS
TREATMENT
- Symptom recognition, prompt treatment – “time is muscle - myocardium”
- Oxygen, antiplatelet- aspirin, nitrates, pain meds, beta blockers, anticoagulation therapy
- Reperfusion – reestablish blood flow
- Cardiac rehabilitation programs
ACS
TREATMENT- REPERFUSION
– Thrombolytic drugs
– Percutaneous coronary intervention (PCI) balloon angioplasty, stenting, artherectomy
– Coronary artery bypass graft (CABG) -surgical revascularization
post infarction
acute inflammatory response (area of necrosis) – 2-3 days
* Necrotic cells replaced with granulation and scar tissue
* Necrotic area soft, yellow – 4-7 days
* Necrotic tissue replacement – 7 weeks
3 zones of tissue damage
post infarction
– Necrotic zone
– Surrounding zone of injured/hypoxic cells , some recovery
– Outer zone ischemic – salvageable cells
Complications - MI
part 1
- Dysrhythmias
- Sudden cardiac death
- Cardiogenic shock
- Heart failure
- Arrhythmias
Complications - MI
part 2
- Ventricular, valve, interventricular septal rupture
- Pericarditis
- Aneurysms
- Stroke
Cardiomyopathy
- Disorders of myocardium – (mechanical and/or electrical)
- Primary or secondary
cardiomyopathy
types
– Genetic – Hypertrophic, Arrhythmogenic, Ion channelopathies
– Mixed – Dilated, Restrictive
– Acquired – Myocarditis, Peripartum, Takotsubo
– Idiopathic
Hypertrophic Cardiomyopathy
patho
Left ventricular hypertrophy, disproportionate thickening of the ventricular septum –> abnormal diastolic filling, cardiac dysrhythmias, intermittent outflow obstruction (left ventricle-in 25%)
- Genetic disorder: autosomal dominant
Hypertrophic Cardiomyopathy
clinical manifestations
asymptomatic, dyspnea, chest pain, exercise intolerance, syncope, dysrhythmias
Hypertrophic Cardiomyopathy
diagnosis
echocardiogram, EKG, continuous ambulatory monitoring (Holter monitor), MRI, genetic testing, physical exam may be normal
Hypertrophic Cardiomyopathy
treatment
medical management, medications, pacemakers, AICD; surgical - myectomy/ablation of septum
Acute Infective Endocarditis
patho
infection of the inner surface of the heart and valves
* Bacterial invasion–> valvular vegetation/debris lesions –> emboli –> bacteremia –> destruction of cardiac valves –> valve dysfunction/perforation, abcesses, pericarditis
Acute Infective Endocarditis
risks
ETOH/IV drug use, diabetes, neutropenia, damaged endocardial surface (valvular disease), implantable devices
Acute Infective Endocarditis
common infecting organisms and sites
Common infecting organisms – staphylococcal, enterococci
- Common site – aortic, mitral valves
Acute Infective Endocarditis
clinical manifestations
fever, heart murmur, petechial hemorrhages in skin, nailbeds, mucous membranes, cough arthralgia/arthritis (emboli)
Acute Infective Endocarditis
diagnosis
blood culture
echo
Acute Infective Endocarditis
treatment
eliminate cause - antibiotics, minimize cardiac effects - may require valve replacement, treat effect of the emboli
Valvular Disease – Stenosis, Regurgitation
Heart valves promote unidirectional flow of blood through the heart
Most common: Mitral, aortic
Disturbances in blood flow, turbulence
Valvular Disease – Stenosis, Regurgitation
causes
congenital, trauma, ischemia, infection, inflammation
Valvular Disease – Stenosis, Regurgitation
stenosis
narrowing of orifice, failure of leaflets to open normally –> decreased blood flow –> impaired emptying, increased work demands on heart
Valvular Disease – Stenosis, Regurgitation
regurgitation
Regurgitant valve – does not close properly –> blood flow continues despite valve closure and/or backward flow
valvular disease
heart murmur
– Stenosis – hear murmur when blood shoots through the narrow opening when valve opens
– Regurgitation – when blood leaks back through a valve that should be closed
valvular disease
heart murmur part 2
Mitral regurgitation, stenosis, aortic regurgitation – pulmonary symptoms
* Aortic stenosis – angina, syncope and heart failure
What two tests are used to diagnose infective endocarditis?
blood culture
cbc
echo
ekg
cxr
ct
mri
Abnormal turbulent blood flow through a diseased valve produces what clinical manifestation?
heart murmur
What happens to blood flow in diastole in mitral valve stenosis
in mitral valve stenosis, the valve opening narrows. The heart now must work harder to force blood through the smaller valve opening. Blood flow between the upper left and lower left heart chambers may decrease.
What happens to the left ventricle in aortic valve stenosis?
Over time, aortic valve stenosis causes your heart’s left ventricle to pump harder to push blood through the narrowed aortic valve. The extra effort may cause the left ventricle to thicken, enlarge and weaken. If not addressed, this form of heart valve disease may lead to heart failure
Does mitral valve regurgitation result in a decreased stroke volume?
The physiologic consequences of mitral regurgitation include reduced forward stroke volume
What valvular problem does the nurse anticipate if the chordae tendinae rupture as a complication of MI?
CTR is characterised by sudden onset, rapid progression of pulmonary edema, hypotension, and left-sided heart failure which may finally lead to severe cardiac shock or pulmonary hypertension and acute right-sided heart failure
Adequate Perfusion
- Pumping ability of the heart
- Intact vascular system to transport blood
- Sufficient blood to fill the vascular system
- Tissues that can extract O2 and nutrients
Heart Failure in Adults
Failure of the heart to deliver sufficient blood to meet the metabolic needs of tissues/cells
* Decrease in cardiac output and the body’s attempt to compensate
Major causes: MI, HPT
* Chronic disorder –> requires continuous treatment with medications
heart failure in adults
characteristics
– Ventricular dysfunction – pump doesn’t work, or a filling problem
– Can reduce ejection fraction
– Reduced cardiac output
* Signs of inadequate tissue perfusion
* Signs of fluid volume overload
aca/aha stage vs nyha functional classification
stage a = n/a classification
high risk for hf
no structural heart disease
no symptoms of hf
acc/aha stage vs nyha functional classification
stage b = class i
b. structural heart disease without symptoms of hf
i. asymptomatic
acc/aha stage vs nyha functional classification
stage c = class ii and iii
c. structural heart disease with prior or current hf symptoms
class ii. symptomatic w/ moderate exertion
class iii. symptomatic with minimal exertion
acc/aha stage vs nyha functional classification
stage d = class iv
d. advanced structural heart disease with marked symptoms of hf at rest despite maximal medical therapy requiring specialized interventions like heart transplant or mechanical assist device
iv. symptomatic at rest
What are signs of inadequate tissue perfusion?
pallor
pain/discomfort
diminished/absent pulse
delayed capillary refill
cyanosis
numbness
loss of motor function
What are signs of fluid retention/volume overload?
Rapid weight gain.
Noticeable swelling (edema) in your arms, legs and face.
Swelling in your abdomen.
Cramping, headache, and stomach bloating.
Shortness of breath.
High blood pressure.
Heart problems, including congestive heart failure
compensatory mechanisms of the heart
frank starling mechanism
myocardial hypertrophy and remodeling
sympathetic reflexes
renin angiotensin aldosterone mechanism
higher levels of natriuretic peptide indicate what
worsening hf
frank starling mechanism
the heart’s physiological ability to change its contraction force, and therefore stroke volume, in response to changes in venous return
myocardial hypertrophy and remodeling mechanism
Cardiac hypertrophy is a common type of cardiac remodeling that occurs when the heart experiences elevated workload. The heart and individual myocytes enlarge as a means of reducing ventricular wall and septal stress when faced with increased workload or injury.
sympathetic reflexes mechanism
Sympathetic vasoconstrictor reflexes are essential for the maintenance of arterial blood pressure in upright position. It has been generally believed that supraspinal sympathetic vasoconstrictor reflexes elicited by changes in baroreceptor activity play an important role.
renin angiotensin aldosterone mechanism
The RAAS is a complex multi-organ endocrine (hormone) system involved in the regulation of blood pressure by balancing fluid and electrolyte levels, as well as regulating vascular resistance & tone. RAAS regulates sodium and water absorption in the kidney thus directly having an impact on systemic blood pressure.
cardiac remodeling post MI
After myocardial infarction (MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction.
expansion of infarct
hours to days
global remodeling
days to months
right ventricular failure
clinical manifestations
congestion of peripheral tissues
dependent edema and ascites
liver congestion
signs related to impaired liver function
gi congestion
anorexia
gi disease
weight loss
left ventricular failure
clinical manifestations
decreased cardiac output
activity intolerance
signs of decreased tissue perfusion
pulmonary congestion
impaired gas exchange
cyanosis
signs of hypoxia
pulmonary edema
cough with frothy sputum
orthopnea
paroxysmal nocturnal dyspnea
heart failure
diagnosis
h and p
labs
ekg
cxr
echo
heart failure
labs
b type natriuretic peptide
heart failure
treatment goals
recting cause, improving cardiac function, maintaining fluid volume, developing activities within individual limitations of cardiac reserve
heart failure
treatment
meds
o2
ventilator support
aicd
ventricular assist devices
heart transplant (end stage failure)
What are two common causes of heart failure?
cad
diabetes
high bp
obesity
Where does blood back up in right sided heart failure?
veins
Where does blood back up in left sided heart failure?
pulmonary veins toward the organs
Left sided heart failure will primarily present with symptoms related to what system
respiratory
what might an increase in dyspnea on exertion tell you about heart failure
it is progressing and that co does not increase sufficiently
What tests are used in the diagnosis of heart failure?
blood work
cxr
ecg
ekg
echo
ef
stress test
ct
mri
Why would the nurse instruct a client with heart failure to weigh themselves daily
to detect worsening HF early and avoid complications.
What causes pulmonary edema?
too much fluid accumulates in the lungs, interfering with a person’s ability to breathe normally
hemodynamics
how your blood flows through your arteries and veins and the forces that affect your blood flow. Normally, your blood flows in a laminar (streamlined) pattern. It flows fastest in the middle of a blood vessel, where there’s no friction with blood vessel walls
dvt
condition that occurs when a blood clot forms in a deep vein. These clots usually develop in the lower leg, thigh, or pelvis, but they can also occur in the arm
The Heart, Part 1 - Under Pressure: Crash Course Anatomy & Physiology #25
https://www.youtube.com/watch?v=X9ZZ6tcxArI
The Heart, Part 2 - Heart Throbs: Crash Course Anatomy & Physiology #26
https://www.youtube.com/watch?v=FLBMwcvOaEo
The (BLANK) is the largest artery in the body.
AORTA
The cardiovascular system is responsible for transporting oxygen, nutrients, and hormones throughout the body.
TRUE OR FALSE
TRUE
Which of the following is responsible for regulating heart rate?
Purkinje fibers
SA node (sinoatrial node)
Bundle of His
AV node (atrioventricular node)
SA NODE (SINOATRIAL NODE)
What is the average resting heart rate for adults?
More than 200 beats per minute
100-150 beats per minute
60-100 beats per minute
30-60 beats per minute
60-100 BEATS PER MINUTE
The (BLANK) are the lower chambers of the heart.
VENTRICLES
The (BLANK) is the main organ of the cardiovascular system.
HEART
What is the role of valves in the cardiovascular system?
To create blood cells
To control heart rate
To regulate blood pressure
To prevent backward flow of blood
To prevent backward flow of blood
Which chamber of the heart receives oxygenated blood from the lungs?
Left atrium
Left ventricle
Right atrium
Right ventricle
LEFT ATRIUM
PULMONARY ARTERY
Carries deoxygenated blood from the heart to the lungs
AORTA
Carries oxygenated blood from the heart to the rest of the body
CAPILLARIES
Microscopic blood vessels where gas exchange occurs
VEINS
Carry blood back to the heart
What is the medical term for high blood pressure?
Hypotension
Atherosclerosis
Arrhythmia
Hypertension
HYPERTENSION
MEDICAL - How cholesterol clogs your arteries (atherosclerosis)
https://www.youtube.com/watch?v=fLonh7ZesKs
