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BNKN602- Exam > cardiac > Flashcards

cardiac Flashcards

1
Q

What is cardio vascular disease

A

any condition that affects the structure and function of the heart and blood vessels

  • coronary artery disease (CAAD)- angina, myocardial infarction
  • cerebrovascular disease (CVD)
  • peripheral vascular disease (PVD)
  • heart failure
  • rheumatic fever disease
  • congenital heart disease
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2
Q

Rheumatic fever

A
  • An autoimmune disease that results from a group A streptococcus (GAS) infection in the throat
  • is linked to poor housing condition, overcrowding, socioeconomic deprivation, barriers to primary health care access and lack of treatment for strep throat
  • if untreated it may develop into rheumatic heart disease and go onto damage the heart, valves may need to be placed
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3
Q

ischemic heart disease (IHD)

A
  • occurs when there is insufficient blood flow and volume to supply the 02 needs of the myocardium
  • cardiac muscle is constantly active requires continues blood supply and oxygen to survive
  • the underlying pathophysiology is usually atherosclerosis
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4
Q

angina

A
  • angina is the symptom of reversible myocardial ischemia
  • angina is usually predictable/ manageable
  • it occurs due to stable lesion/ plaque in the coronary artery
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5
Q

key pathophysiology of IHD

A

ineffective myocardial oxygen perfusion
- myocardial oxygen demand is greater then oxygen supply
- at risk of heart muscle damage/ necrosis
damaged muscle doesnt work effectively
- at risk of arrhythmia (damaged muscle doesnt convey impulses well)
- may lead to cardiac arrest

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6
Q

myocardial infarction

A
  • results from sustained ischemia or sudden complete blockage of the coronary artery
  • myocardial tissue distal to the obstruction dies
  • can be partial thickness (NSTEMI) or full thickness (STEMI)
  • life threatening
  • complications include cariogenic shock, heart failure, ventricular fibrillation (VF) and death
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7
Q

MI is defined as

A
  • non ST-elevation myocardial infarction (NSTEMI) involves partial thickness myocardial wall damage
  • ST-elevation myocardial infarction (STEMI) involves full thickness myocardial wall damage with/ without narcosis
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8
Q

STEMI

A
  • full thickness damage to myocardium (transmural)
  • sudden complete blockage of a coronary artery
  • ST segment elevation on an ECG
    no need to wait for bloods ECG findings is definitive
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9
Q

NSTEMI

A
  • partial thickness damage to the myocardium
  • partial blockage of the coronary artery
  • not visible on an ECG
  • need bloods for cardiac biomarkers to diagnose
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10
Q

Acute coronary syndrome (ACS)

A
  • group of clinical symptoms that are consistent with acute myocardial ischemia. unless interventions are applied promptly ACS can result in myocardial death
    ACS is the term for an imbalance of 02 supply and demand. the underlying pathophysiology is atherosclerosis which can lead to plaque rupture and thrombus formation
  • unstable angina pectoris
  • STEMI
  • non-STEMI
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11
Q

ACS

A
  • thrombus formation may occlude the coronary artery leading to anaerobic metabolism and potential death
  • pain may be different to usual angina pain
  • ACS can occur without percipients
  • unrelieved by the individuals usual methods of symptom relief
  • lasts longer then 20 minuets
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12
Q

precipitants of angina/ ACS myocardial oxygen demand thats not being met

A

exercise/ excretion
- increased HD, increased CO, increased myocardial 02 demand
extreme temperatures
- vasocontraction increases resistance
- vasodilation decreases venous returns
eating a heavy meal
- increase parasympathetic stimulation (blood diverts to the GI system)
emotions/ stress (SNS increase HR increases, heart works harder)
- increased HR, increased CO, increased myocardial 02 demand
effect of drugs
- can increase/ decreased HR and BP

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13
Q

signs and symptoms of IHD, ACS

A

Pale, grey, confused, tachycardic, hypotensive, hypertensive, chest pain, dyspnoea, weak thready pulse, feeling of impending doom, think it’s indigestion, feel like an elephant on their chest, tachypneic, fatigue, anxiety, ECG abnormalities, pain radiating across the chest, down the left arm, into the jaw, into the back, palpitations, restlessness, tightness in chest, hypoxaemia, diaphoresis, cyanosis, dizzy, light-headed, nausea

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14
Q

minimising the effects of MI

A
  • in absence of 02, cell function will deteriorate
  • ischemia: lack of 02
  • injury: potential reversible damage
  • infarction: necrosis- permanent damage
    intervene early
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15
Q

ACS/ MI is diagnosed by:

A
  • history- chest pain and related symptoms
  • 12 lead ECG- ST elevation height and area of heart
  • blood tests
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16
Q

Blood tests

A
  • Troponin T and I- cardiac specific enzymes
  • Cardiac enzymes: creatinine kinase (CK- MB) - mainly in cardiac muscle, myoglobin- cardiac and skeletal muscles
  • Electrolytes - K+, NA+, important for electrical conduction and kidney function
  • Full blood count (FBC)
  • Lipid profile- fasting
  • Brain naturide peptide (BNP) released when ventricles are under stretch (
  • Creatinine clearance time (renal impairment - dosing)
  • May do a CRP- inflammation
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17
Q

other diagnostic investigations that may be undertaken include:

A
  • coronary angiogram +/- angioplasty
  • echocardiography (ECHO) ultra scan of the heart
  • transesophageal test (ETT) looks at back of the heart)
  • electrophysiological studies (EPS)
  • CXR (not always, if someone has hear failure looking at size of the heart)
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18
Q

priority goals in management

A

Open the artery and keep it open (myocardium needs oxygen)

  • Increase oxygen supply to the myocardium - give nitrates and consider 02 if. Sa02 <93%
  • Relieve pain, reduce 02 demand and signs of ischemia
  • Preserve viable myocytes
  • Relieve obstruction
  • Manage thrombus to reperfusion the artery and minimize permanent damage
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19
Q

interventions for ACS

A
  • Follow the heart foundation angina action plan
  • Percutaneous coronary interventions (PIC) the gold standard
  • Thrombolysis- fibrinolytic therapy (dissolves clots)
  • Alteplase/ metalyse
  • Streptokinase
    Tissue plasminogen activator (TPA)
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20
Q

Heart attack

A

Heart attack Is a MI
- Results from a blocked coronary artery
- This prevents oxygen-rich blood from reaching the myocardium
- Without oxygen the myocardial cells begin to die
A circulation problem

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21
Q

cardiac arrest

A

Cardiac arrest a sudden cessation of the hearts functioning
- Triggered by electrical malfunction in the heart that causes an arrhythmia (irregular heart beat)
- Disrupts the pumping action
An electrical problem

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22
Q

cardiac output

A

SV X HR (3.5L/min)

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23
Q

stroke volume (SV)

A

the amount of blood pumped out per heart beat

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24
Q

preload

A

(volume) amount of ventricular stretch at the end of diastole. the greater the stretch the stronger the contraction

25
Q

What is heart failure

A
  • HF is the hearty inability to consistently pump enough blood to organs and tissues
  • Cardiac output is insufficient to meet the metabolic demands of the body and accommodate venous return
  • Occurs from either a structural or functional abnormality of the heart
  • The resulting decreased blood supply to the body impairs organs and tissue function
  • The dominant feature is inadequate tissue perfusion
  • Case of under perfusion
  • Structural= valve problem/dysfunction, ventricles thickness, rigidity
  • Function= following a MI, cardiomyopathy, CAD
  • Primarily a disease of elderly- 6-10% >65 will have diagnosis HF
26
Q

signs and symptoms of heart failure

A
  • Pale, grey, SOBOE, orthopnea, nocturia, oedema, confusion, tachycardia, hypotensive, dry cough, dyspnoea, weak pulse, tachypnoea, fatigue, anxiety, ECG abnormalities, palpitations, restlessness, hypoxaemia, moist cough, diaphoresis, cyanosis, dizzy, light headed, nausea, weight gain, SOB, crackles on auscultation
  • Not all present in one person
  • Many similar to IHD, ACS
  • Need to assess well can not assume
  • Might be PE ect consider differential diagnosis
  • Orthopnea- unable to lie flat
  • Nocturia- increased urination overnight due to lying flat and kidneys being well perfused
  • Oedema- fluid in tissues have seen it in elbows
27
Q

systole

A

Systole = the ventricles eject blood (PUMP)
- Systolic HF
- Heart failure reduced ejection fraction (HFREF)
- Pumping problem
Inability of the ventricle to contract effectively

28
Q

diastole

A

Diastole
Diastole= the ventricles fill with blood (RELAX)
- Diastolic HF heart failure preserved ejection fraction (HFPEF)
- Relaxation problem
- Inability of the ventricles to relax and fill effectivley

29
Q

normal diastole

A

ventricles fill with blood and pump it out

30
Q

normal systole

A

pumping 60% and more out into lungs & body

31
Q

systolic failure

A

(HF REF) – enlarged ventricles fill, but cannot fully empty out all of blood, ventricle pumping down to 40 %

32
Q

diastolic failure

A

(HF PEF) – stiff ventricles unable to relax and fill, can efficiently pump out blood up to 70 %, but not filling with enough blood initially

33
Q

left heart failure

A

Left ventricle (LV) cannot pump blood effectively to the systemic circulation. The blood backs up in the pulmonary system so the pulmonary venous pressure increases resulting in

  • Deceased EF
  • Pulmonary congestion/ oedema with dyspnoea
  • Cough
  • Crackles
  • Impaired oxygen exchange
34
Q

right heart failure

A

The right ventricle (RV) cannot eject sufficient amounts of blood- blood backs up in the venous system and may result in:

  • Peripheral oedema
  • Weight gain but anorexia/nausea may be present
  • Hepatomegaly/ splenomegaly
  • Ascites
  • Jugular vein distension
35
Q

compensatory mechanisms heart failure

A
  • Baroreceptors (pressure sensors) in the aortic and carotid arteries sense a drop in BP
  • The sympathetic nervous system (SNS) releases adrenaline and noradrenaline
  • Low cardiac output and vasoconstriction results in decreased renal perfusion -> renin is released by the kidneys
  • This initiates the renin angiotensin aldosterone system (RAAS)
    SNS response is short lived, hard work & damaging to the ventricles, aim is to increase BP by increasing HR and thus circulating blood volume
    1. SNS activation results in
    - Increase heart rate increased contractility which increased blood pressure
    2. Neuro-hormonal activation results in
    • Increase blood volume(related to aldosterone and ADH secretion) which increases preload angiotensin 11 decrease vascular capacity which increases afterload
36
Q

consequences for heart failure

A

Pathophysiological process
- Decrease in blood and 02 supply to body (pumping failing)
- SNS and RAAS response helps…. But ultimately harms
Signs and symptoms
- Shortness of breath
- Orthopnea/ nocturia
- Oedema- peripheral/ pulmonary
- Exercise intolerance
- Fatigue
- Weight gain
- Attempts to increase cardiac output to increase 02 delivery:
- Tachycardia (risk of arrythmias increased)
- Tachypnoea

37
Q

chronic heart failure

A
  • Heart failure is commonly caused by IHD
  • It is common in the elderly- one of the main reasons for admission to hospital
  • The pathological process that underpin heart failure result in decreased contraction, decreased filling or both
38
Q

difference between acute and chronic HF

A

ACUTE i.e. post surgery fluid overload – common in the elderly – correct the cause with diuretics and it goes away
CHRONIC i.e. r/t myocardial dysfunction caused by IHD, cardiomyopathy, HTN or valvular disease/disorders

39
Q

how to know if someone has HF

A 
Statements of:
- c/p, heavy weight, indigestion, SOB, SOBOE, 
- Increased HR (to pump more oxygen around body) 
- BP low
- Ability to speak
- ECG
- Oxygen saturations and/or ABG
- Cyanosis/colour/diaphoresis 
- Sounds (gurgling/snoring/apnoea) 
- Agitation/confusion
- Anxiety
Dyspnoea
40
Q

assessments for HF

A
  • Rapid Ax, Posterior Chest Ax, Peripheral vascular Ax, Apical pulse – PMI, if sound displaced then eg of ventricular hypertrophy
41
Q

diagnostics interventions

A
  • CXR- cardiomegaly
  • ECG- arrhythmias- St changes
  • Echocardiogram - LV dysfunction, EF%
  • JVP
  • Neurohormone’s- brain natriuretic peptide (BNP) increase
  • Exercise tolerance test
  • Cardiac catheterization
  • Blood studies
  • BNP electrolytes, full blood count (FBC), TNI, cardiac enzymes, liver, thyroid function- other cause?
42
Q

management of HF

A

Management
Treat the underlying cause if possible
- Aim to increase cardiac function and decrease myocardial workload- beta blockers ect. - Prevent harmful neuroendocrine responses e.g. SNS, RAAS, ventricular remodeling- ACE inhibitors
- Manage with medication, daily weight, 02 if required, fluid restriction, low sodium diet and other lifestyle modifications
- The nurse has a role in education and management of symptoms

43
Q

main goal HF

A

MAIN GOAL – TREAT UNDERLYING CAUSE ie MI, valve dysfunction, ischaemia

  • Contributing factors, maximize cardiac output, provide treatment to alleviate - symptoms
  • Improve ventricular function
  • Preserve organ function
  • DECREASE intravascular volume
  • Decrease venous return [preload]
  • Decrease afterload [resistance against which LV must pump]
44
Q

what is the kidney responsible for

A
  • Acid-base balance
  • Water balance
  • Electrolyte regulation
  • Toxin regulation
  • Toxin removal BP regulation
  • Erythropoietin production -> RBC production in the bone marrow
    Vitamin D activation
45
Q

glomerular filtration rate

A
  • Glomerular filtration rate (GFR) is the amount of blood that passes through the glomeruli each minute
  • The normal blood flow through the kidneys is 105-125 mls/min -> 99% is reabsorbed resulting in 1-1.5L of urine per 24 hours
  • The GRF is usually estimated and written as eGFR
46
Q

factors needed for urine output

A

Pre-renal
- Adequate perfusion pressure (renal blood flow) and oxygenation of kidneys
Renal
- The kidney units must be functioning properly i.e. no damage to the structure in the kidney such as tubules, glomerular
Post-renal
- There must be no obstruction to urine flow
Oliguria and anuria
- Oliguria = 100- 400 ml/day (low urine output)
- And early warning sign related to poor urine output
- Anuria = <100ml/day
- Late warning sign related to poor urine output
- Absolute anuria = nill
TWO HOURS OF OLIGURIA CAN CAUSE ACUTE KIDNEY INJURY

47
Q

acute kidney injury

A
  • Acute kidney injury (AKI) occurs when the kidneys are unable to remove the body’s metabolic water or perform their seven regulatory functions- in particular, for cardiac week, maintenance of BP and electrolyte regulation
  • These metabolic wastes build up in the body
  • GFR falls as the disease progresses
    Rapid loss of renal function due to kidney damage- can be life threatening
48
Q

pre-renal causes

A
  • Low CO, low BP, severe vomiting
49
Q

intrarenal (intrinsic) causes

A
  • Damage to renal tissue, nephrotoxins, NSAIDS
50
Q

4 phases kidney injury

A
  • Initiating phase hours- days
  • Oliguric phase 10 -14 days
  • Diuretic phase
  • Recovery phase 3-12 months
51
Q

nursing assessment kidney

A
  • Fluid balance chart (FBC)
  • Daily weigh (1kg of weight= 1L retained fluid)
  • Skin integrity
  • Vital signs -. EWS
  • Capillary refill time (CRT)
  • Palpate and/ or scan the bladder
  • Bloods- BFR, electrolytes, CBC
  • Ability to manage Adl’s
52
Q

treatment aims kidney injury

A
  • Aim to prevent it altogether (high mortality rate)
  • Determine the cause and treat it e.g. manage MI, or give IV fluids ect
  • Supportive care while unwell- rest is important
53
Q

kidney injury progress to end stage kidney disease (ESKD)

A
  • BFR <15ml/min
  • Requires renal replacement therapy (RRT) dialysis or transplantation
  • 2 types of dialysis
  • Hemodialysis
  • Peritoneal dialysis
54
Q

cardiac rhythms

A
  1. Normal sinus rhythm
  2. Arrhythmias such as
    - Ventricular tachycardia (VT)
    - Ventricular fibrillation (VF)
    - VT and VF are life threatening rhythms
  3. Asystole absence of any rhythm at all
  4. Atrial fibrillation (AF) - this is a common arrhythmia you may see out in clinical
55
Q

ventricular tachycardia

A
  • Ventricular tachycardia (VT) is characterized by absence of P waves as the ventricles have taken over - QRS complex is wide and fast
  • There is initially a pulse, but VT can progress onto no palpable pulse (no cardiac output) -> cardiac arrest (needs defilation)
  • This is a life threatening rhythm
56
Q

ventricular fibrillation

A
  • Ventricular fibrillation (VF) is characterized by rapidly disorganized contraction of the ventricles= life threatening rhythm- needs defibrillation immediately
  • No discernible atrial or ventricular activity
  • No palatable pulse (no cardiac output) or respirations= cardiac arrest
  • VF is the most common arrythmia in patients with cardiac arrest- can be because of a myocardial infarction (MF)
57
Q

asystole

A
  • Easiest rhythm to memories
    • Complete absence of electrical activity- straight line on the monitor
    • No BRS complexes = no cardiac output
    • Cessation of the hearts functioning
    • Cannot defibrillate this
      This needs adrenaline, to cause VF and then you shock you out of it
58
Q

atrial fibrillation

A
  • Atrial fibrillation (AF) completely disorganized atrial electrical activity
  • Impulses arise from the SA nose and other sites in the atria
  • Conduction through the AV nose is irregular and usually fast
  • There are no P waves and it is irregular
  • Instead of a P wave- it has uneven fibrillation lines (f waves) before the QRS complex
59
Q

12 lead ECG

A
  • A diagnostic tool used to help identify pathological changes associated with acute coronary syndromes (ACS) such as a myocardial infarction (MI)
  • Detects the hearts electrical activity through electrodes attached to the skin and relays them as waveform for interpretation on graph paper
  • 10 physical leads to attach to the patient showing 12 different views of the heart

BNKN602- Exam (5 decks)

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